Child Nutrition and Health

CHILDREN'S ISSUES, LAWS AND PROGRAMS
CHILD NUTRITION AND HEALTH
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CHILDREN'S ISSUES, LAWS AND PROGRAMS
CHILD NUTRITION AND HEALTH
GREGOR CVERCKO
AND
LUKA PREDOVNIK
EDITORS
New York
Copyright © 2013 by Nova Science Publishers, Inc.
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LIBRARY OF CONGRESS CATALOGING-IN-PUBLICATION DATA
Child nutrition and health / [edited by] Gregor Cvercko and Luka Predovnik.
pages cm
Includes bibliographical references and index.
ISBN: (eBook)
1. Children--Nutrition. 2. Children--Health and hygiene. I. Cvercko, Gregor. II. Predovnik, Luka.
RJ206.C513 2013 618.92--dc23
2012035888
Published by Nova Science Publishers, Inc.  New York

Contents
Preface vii
Chapter I Nutrition in Children and Adolescents with Cancer 1
Terezie Tolar Mosby and Ronald D. Barr
Chapter II Calcium Supplementation in Young Children
in Asia: Prevalence, Benefits and Risks 43
Shu Che, Colin Binns and Bruce Maycock
Chapter III Exposure of Slovenian Preschool Children to Preservatives
and Polyphosphates 67
Elizabeta Mičović, Mario Gorenjak,
Gorazd Meško and Avrelija Cencič
Chapter IV The Breakfast Experience in Low Socioeconomic
Families with Overweight Children 89
Simone Pettigrew and Melanie Pescud
Chapter V Early Vitamin D Supplementation,
Immune Modulation and Allergy 107
Gian Vincenzo Zuccotti and Valeria Manfredini
Chapter VI Factors Associated with Overweight and Obesity
among Kuwaiti Young Children 121
A. N. Al-Isa, Nadeeja Wijesekara,
Ediriweera Desapriya and Yamesha Ranatunga
Index 137
Preface
In this book, the authors have gathered and present current research in the study of child
nutrition and health from across the globe. Topics discussed include the exposure of
Slovenian preschool children to preservatives and polyphosphates; the breakfast experience in
low socioeconomic families with overweight children; nutrition in children and adolescents
with cancer; calcium supplementation in young children in Asia; early vitamin D
supplementation, immune modulation and allergy; and the factors associated with overweight
and obesity among Kuwaiti young children.
Chapter I - Cancer is the most common cause of disease-related death in children and
adolescents in the United States, and it is becoming a proportionately more common cause of
death among young people in developing countries as well. However, cancer is highly curable
in young people. In high income countries, the survival rate of children and adolescents with
cancer is 80% or higher. However, more than 80% of children live in low and middle income
countries where the survival rate may be as low as 5%. Nutrition plays an important role in
many aspects of cancer development, treatment and long term survival.
Nutritional status at diagnosis has prognostic implications. Well-nourished children have
a better tolerance of intensive cancer therapy, improved chances of survival, and lower
relapse rates. Children and adolescents with cancer are at higher risk for the development of
malnutrition than adults during treatment due to the relatively higher nutritional needs
demanded by their continuous growth and organ development.
Nutritional assessment is important for the prevention, recognition, and early treatment of
malnutrition. Proper assessment of the nutritional status of a patient is necessary for the
determination of appropriate nutritional therapy.
The goals of nutritional therapy for patients undergoing anticancer treatment are to
maintain weight and to achieve age-appropriate growth and weight gain after treatment.
These goals can be achieved by dietary modifications, use of dietary supplements, appetite
stimulants, or nutritional support. Patients undergoing chemotherapy, radiation and
hematopoietic stem cell transplantation can experience any or all of the following side effects:
nausea, vomiting, mouth sores, constipation, diarrhea, altered taste, loss of appetite. Any of
these side effects could result in undesirable weight loss, protein energy malnutrition or
cancer cachexia. Food poisoning can occur if a person eats or drinks something that contains
harmful germs. Food consumed by immunocompromised patients should be prepared in a
manner to minimize bacterial growth.
viii Gregor Cvercko and Luka Predovnik
Survivors of cancer in childhood and adolescence are at risk for many long-term adverse
effects of therapy. Lifestyle changes, including dietary modification, may help with the
management of some of those sequelae. The three nutrition-related key areas to reduce cancer
risk are weight, diet, and physical activity.
There are numerous gaps in our knowledge concerning the interaction of nutrition with
cancer in children and adolescents. These include the effects of nutritional interventions on
cancer outcomes and the influence of such interventions on co-morbidities; all providing rich
opportunities for good clinical research.
Chapter II - Calcium is essential for maintaining bone health in infants and young
children. The calcium intakes of weaning infants and children in Asia are relatively low in
comparison to their Western counterparts. This is an increasing concern for Asian parents and
is one reason the Asia Pacific region is becoming a large market for vitamins and dietary
supplements. However, there is a lack of data on the long-term benefits to early calcium
supplementation of healthy infants and young children.
The objective of this chapter is to discuss the appropriate calcium intakes for infants and
young children, the risks and benefits of calcium supplementation and to review the
proportion of children in Asia who are taking calcium supplements. To achieve our objective
a literature review was undertaken of the English language databases PubMed and Web of
Knowledge. Studies were selected that reported outcomes of calcium intake in infants and
young children, as well as systematic reviews of such studies.
Studies were undertaken of children in China and a comparison group of Chinese
children living in Australia to document the use of calcium supplements. The prevalence of
dietary supplementation among children under five years old in China (30.0%) was higher
than in Australia (21.6%). In supplement users in China, 60.3% of them took calcium
supplementation while only a small number in Australia (8%) took calcium supplements. Age
and feeding method of the child (ever breastfed or not) were associated with nutritional
supplementation in Australia, while household income and mother’s educational status were
significantly related to the use of dietary supplements including calcium supplements in
China. More than half of the children took supplemental calcium in the form of calcium
gluconate (51.8%) and the average intake from supplements was 131 mg per day.
There is little evidence to support the general use of calcium supplements in infants who
were exclusively breastfed or formula fed. Evidence from recent studies does not support the
use of calcium supplementation in healthy children as a public health intervention. However,
for weaning infants and children with low calcium intakes, increased intake of calcium-rich
foods should be encouraged. If adequate calcium cannot be achieved through food sources,
supplementation may be an effective alternative. More studies are required in infants and
young children with low calcium intakes, particularly those living in Asian countries or
children of Asian ethnic origin.
Chapter III - The purpose of this chapter is to present exposure of preschool children to
daily consumed food preservatives and polyphosphates: sorbic acid, benzoic acid, nitrate,
nitrite, sulphur dioxide and polyphosphates. For exact exposure of chemicals in food, data of
consumed food intake and concentration of observed chemicals in food are needed.
Methodology: Among the randomly selected regions in Slovenia, we randomly selected
kindergartens and children aged from 2-6 years. The study included 190 children, 98 boys and
92 girls. Anthropometric measurements of children were conducted, so data on the sex, age,
measured weight and height of the children were available. The dietary intake was based on
Preface ix
the 3-day-weighed record method. The data from databases obtained from the official control
and monitoring of food additive content in consumed food were used to calculate estimated
daily intake (EDI). Such estimated exposure of each preservative and polyphosphates EDI
was compared with acceptable daily intake (ADI) and expressed as % of ADI. Results:
average exposure to each preservative and polyphosphates EDI was not exceeding ADI. It is
evident that average exposure to nitrites and sulphur dioxide is relatively high, while intake of
benzoic acid, sorbic acid, nitrates and polyphosphates is not so high. The mean daily exposure
of children to nitrites ranged from 12.8 % to 28.3 % ADI, to sulphur dioxide from 14.3 % to
21.4 % ADI, while to sorbic acid from 3.8 % to 4.5 % ADI and polyphosphates from 1.8 % to
3.9 % ADI.
It is apparent that such exposure does not present any harm or threat to observed children
although we should consider the fact that ADI for sum of preservatives and polyphosphates
have not been set yet.
Chapter IV - Dietitians emphasise the importance of a healthy breakfast as part of a
balanced diet. As well as providing energy to fuel physical and mental activity, there is
increasing evidence that eating breakfast assists individuals manage their food intake to
prevent excessive weight gain. Parents play a critical role in determining if their children eat
breakfast and, if so, the kinds of foods that are consumed at this meal. Limited previous
research has specifically examined parents’ beliefs and behaviours in relation to this aspect of
their children’s diets. Such information is especially important in the context of low
socioeconomic families given that disadvantaged children have significantly higher rates of
overweight and obesity and poorer academic performance relative to their more advantaged
peers. In the present study, parents’ attitudes to breakfast and its role in children’s health were
explored. A range of qualitative data collection methods was employed over an extended
period (12 months) with low socioeconomic status parents of overweight children. Insights
were generated into the barriers, motivators, and facilitators influencing whether parents
provide their children with healthy breakfasts. Numerous factors were listed as making it
difficult to ensure children eat a healthy breakfast. These included time constraints, children’s
taste preferences, a lack of appetite upon waking, and a reluctance among some parents to
model recommended breakfast consumption behaviours. The findings indicate that future
efforts to improve children’s nutrition could (i) build on parents’ existing belief that breakfast
is important and (ii) suggest coping strategies for parents to overcome the identified barriers
to selecting and serving healthy breakfast foods.
Chapter V - A daily Vitamin D (VitD) intake of at least 400 IU/day is recommended
nowadays by most updated guidelines during the first year of life. However, it is not known
whether such an intake is enough to provide all the health benefits associated with VitD and a
consensus is still missing stating the serum vitD levels appropriate for global health and the
cutoffs for deficiency in younger individuals.
Potent immune-modulating effects of VitD have been reported in vitro and, in particular,
its potential ability to influence both innate and adaptive immunity, reducing the
inflammatory response associated with Th1 and Th17 cells and skewing the T cell balance
towards a Th2-phenotype.
VitD immune-modulation activities could thus play a role in controlling infections and
reducing inflammatory responses toward viral pathogens in both children and adults.
However, the evidence in relation to vitD and allergic diseases is controversial.
x Gregor Cvercko and Luka Predovnik
Most evidence report a protective effect of vitD against allergy. Some studies, however,
suggest that VitD supplementation can be a risk factor for asthma and atopic disorders,
assuming that VitD could induce sensitization against allergens during infancy.
In this chapter, published data on the relationship between vitamin D and asthma and
allergy will be discussed, emphasizing the need for controlled, prospective studies on vitamin
D supplementation to clarify whether it has a role in the prevention of and treatment for
asthma and allergic conditions.
Chapter VI - Background. Childhood obesity is becoming a global epidemic which may
result in increased morbidity and mortality during young adulthood. Objectives. To identify
common factors associated with overweight and obesity among Kuwaiti intermediate school
children aged 10-14 years to support Kuwaiti obesity prevention policy making. Methods.
Weights and heights of 343 female and 340 male students were collected to obtain body mass
index (BMI). Results. The prevalence of overweight and obesity were 21.9 and 6.4% among
females and 22.9 and 7.6% among males, respectively. Risk factors for obesity in males and
females vary considerably and also differ between age groups. Conclusion. Health education
programs focused on reducing obesity in Kuwait must be multifactorial in nature and should
be defined by gender and age group.
In: Child Nutrition and Health ISBN: 978-1-62257-981-5
Editors: G. Cvercko and L. Predovnik © 2013 Nova Science Publishers, Inc.
Chapter I
Nutrition in Children and Adolescents

with Cancer
Terezie Tolar Mosby1 and Ronald D. Barr2,

1
St Jude Children’s Research Hospital, Memphis, TN, US
2
Departments of Pediatrics, Pathology and Medicine,
McMaster University, Hamilton, Ontario, Canada
Abstract
Cancer is the most common cause of disease-related death in children and
adolescents in the United States, and it is becoming a proportionately more common
cause of death among young people in developing countries as well. However, cancer is
highly curable in young people. In high income countries, the survival rate of children
and adolescents with cancer is 80% or higher. However, more than 80% of children live
in low and middle income countries where the survival rate may be as low as 5%.
Nutrition plays an important role in many aspects of cancer development, treatment and
long term survival. Nutritional status at diagnosis has prognostic implications. Well-
nourished children have a better tolerance of intensive cancer therapy, improved chances
of survival, and lower relapse rates. Children and adolescents with cancer are at higher
risk for the development of malnutrition than adults during treatment due to the relatively
higher nutritional needs demanded by their continuous growth and organ development.
Nutritional assessment is important for the prevention, recognition, and early
treatment of malnutrition. Proper assessment of the nutritional status of a patient is
necessary for the determination of appropriate nutritional therapy. The goals of
nutritional therapy for patients undergoing anticancer treatment are to maintain weight
and to achieve age-appropriate growth and weight gain after treatment. These goals can
be achieved by dietary modifications, use of dietary supplements, appetite stimulants, or
nutritional support. Patients undergoing chemotherapy, radiation and hematopoietic stem
cell transplantation can experience any or all of the following side effects: nausea,
vomiting, mouth sores, constipation, diarrhea, altered taste, loss of appetite. Any of these
side effects could result in undesirable weight loss, protein energy malnutrition or cancer

Room 3N27, Health Sciences Centre. McMaster University, 1200 Main Street West, Hamilton, Ontario, L8S 4J9,
Canada, Tel: 1-905-521-2100 X 73428, Fax: 1-905-521-1703, E-mail: rbarr@mcmaster.ca.
2 Terezie Tolar Mosby and Ronald D. Barr
cachexia. Food poisoning can occur if a person eats or drinks something that contains
harmful germs. Food consumed by immunocompromised patients should be prepared in a
manner to minimize bacterial growth. Survivors of cancer in childhood and adolescence
are at risk for many long-term adverse effects of therapy. Lifestyle changes, including
dietary modification, may help with the management of some of those sequelae. The
three nutrition-related key areas to reduce cancer risk are weight, diet, and physical
activity. There are numerous gaps in our knowledge concerning the interaction of
nutrition with cancer in children and adolescents. These include the effects of nutritional
interventions on cancer outcomes and the influence of such interventions on co-
morbidities; all providing rich opportunities for good clinical research.
A. Introduction
Prevalence of Cancer and Access to Care in High Income and Low Income
Countries
Cancer is the most common cause of disease-related death in children and adolescents in
the United States [1] [2] and it is becoming a proportionately more common cause of death
among young people in developing countries. In the U.S. every year more than 12,000
children (less than 15 years of age) are diagnosed with cancer, with an incidence of 155 new
cases per million [3] In all high income countries combined, 50,000 children are diagnosed
with cancer each year [4]. In low and middle income countries, more than 200,000 children
are diagnosed with cancer annually [4]. Therefore, the great majority of children with cancer
live in the developing world [5]. The most common types of cancers in children in the US are
acute leukemia and brain tumors, which together account for half of all cases [6]. There are
some regional and ethnic differences in cancer incidence which are not well understood but
may suggest genetic predisposition or infectious etiologies [7]. Some examples are the high
incidence of Burkitt lymphoma and retinoblastoma in some African regions [5], the low
incidence of neuroblastoma in Blacks and of Ewing sarcoma in Chinese, and the high
incidence of Kaposi sarcoma in eastern and southern Africa [7].
Malnutrition is the condition that results from an unbalanced diet in which certain
nutrients are lacking - undernutrition, in excess (too high an intake) - overnutrition, or in the
wrong proportions [8], although the term malnutrition is interchanged with undernutrition in
common usage. Undernutrition (malnutrition) is one of the most common causes of death in
children in the developing world. However, it is uncommon in the general population of
children in the United States. Complications of undernutrition before a diagnosis of cancer are
frequent in low-income countries, whereas childhood overnutrition is the more frequent
problem among young people in high-income countries. Both undernutrition and obesity can
affect treatment outcome.
Treatment Outcome
Cancer is highly curable in children and adolescents. In high income countries, their
survival rate is 80% or higher [5]. However, more than 80% of children live in low and
middle income countries where the survival rate may be as low as 5% [5]. Unfortunately, the
Nutrition in Children and Adolescents with Cancer 3
difference in survival for children diagnosed with cancer between high income and low
income countries continues to widen as more advanced therapies are developed in the former
but not implemented in the latter [9]. The low survival rate in low income countries is multi-
factorial in origin and includes limited availability and access to care, abandonment of
treatment, malnutrition and advanced disease at the time of diagnosis. In high income
countries, treatment outcome depends on such factors as the type and extent of disease, and
the method of treatment used.
1. Nutritional Status at Diagnosis
Impact of Over and Undernutrition

Nutritional status at diagnosis has prognostic implications. Well-nourished children have
a better tolerance of intensive cancer treatment, improved chances of survival, and lower
relapse rates [10]. Both undernutrition and overnutrition at the time of diagnosis are
associated with poorer treatment outcome [11] [12]. Malnourished children are at an
increased risk for treatment-related complications, reduced tolerance of therapy, altered drug
metabolism, increased susceptibility to infection, and poorer treatment outcome. They are
also at higher risk for improper physical and psychological development [13] [14]. As they
age, malnourished children may have permanent mental and physical disabilities [15]. The
younger the child, the more severe the effects of malnutrition may be.
I. Undernutrition (Underweight)
It is estimated that the prevalence of malnutrition in children in the general population in
low income countries can range up to 32% in some parts of Africa and up to 43% in India
[16]. The prevalence of malnutrition in low income countries at the time of diagnosis of
cancer depends on the geographical region, type of cancer and method used to diagnose
undernutrition. For example, in Central America, more than 70% of children had some type
of nutritional depletion at the time of diagnosis [17]. Undernutrition was associated with
higher rates of death due to abandonment of therapy and treatment failure [12].
II. Overnutrition (Overweight and Obesity)

Obesity is an increasing problem among children, not just in high income countries but
also in low income countries. It is estimated that, in the US, 20% of children are obese.
Overweight children are taller than their peers, have earlier onset of puberty and are presumed
to be more mature [18]. Childhood obesity is associated with hyperlipidemia, hypertension,
diabetes and insulin resistance, hepatic steatosis, cholelithiasis, pseudotumor cerebri, sleep
apnea, and orthopedic abnormalities [18].
All of those problems can affect treatment outcome. With only a small number of
pharmacological investigations regarding the half-life, volume of distribution, and clearance
of drugs in obese patients, there is the risk of under dosing and/or over-dosing patients
considered to be obese [11].These risks can result in poorer treatment outcome and/or greater
toxicities in these patients [11].
2. Nutritional Status during Treatment
Children and adolescents are at higher risk for the development of malnutrition than
adults during cancer treatment due to the relatively higher nutritional needs demanded by
their continuous growth and organ development. Anti-cancer treatment itself affects the
nutritional status of patients and contributes to malnutrition. It is difficult to estimate the
prevalence of malnutrition during treatment due to the lack of uniform criteria and adequate
studies [19] but rates are estimated to be 0-10% for leukemia, 20-50% for neuroblastoma and
0-30% for other malignancies [19]. Suspected contributing factors are energy deficit,
including low energy intake and increased metabolic rate, inflammation related to cachexia
and malabsorption related to intestinal and other organ damage. The severity and variety of
side effects depends on the nature of the disease and the treatment used. Common side effects
interfering with nutrition are nausea, vomiting, loss of appetite, alteration of taste, mucositis,
pancreatitis, pneumatosis intestinalis, and colitis.
In those who have undergone hematopoietic stem cell transplantation (HSCT), graft
versus host disease (GVHD) may result in an additional nutritional challenge. On the other
hand, prolonged steroid use, physical inactivity and certain changes in metabolism predispose
children with cancer to obesity. Malnutrition precludes optimal healing and recovery from
therapy; therefore maximal effort should be focused on its prevention and treatment.
B. Nutritional Assessment
Nutritional assessment is important for the prevention, recognition, and early treatment of
malnutrition. Proper assessment of the nutritional status of a patient is necessary for the
determination of appropriate nutritional therapy. Special attention should be paid to metabolic
derangements of macronutrients, leading to protein energy malnutrition (PEM), and
micronutrients such as deficiencies of vitamin D, vitamin K, zinc, copper and selenium.
There are many techniques that can be used to evaluate the nutritional status of
adolescents and children. The choice of technique will depend on hospital resources,
diagnosis, type of treatment, and other factors. In any case, both objective and subjective data
should be used to complete the nutritional assessment. One measure alone should not be used
to evaluate nutrition; therefore, healthcare providers should use critical thinking skills to
assess nutritional status.
1. Screening
Screening should be performed within 24-72 hours of admission for every patient and
repeated regularly depending on the patient’s age, diagnosis, treatment, and other risk factors.
Nutritional screening should include weight history, usual body weight, and a subjective
history of current symptoms that includes, but is not limited to, nausea, vomiting, diarrhea,
and appetite. Questions about food availability and who is responsible for food preparation
should be asked as well. Such screening can identify children who are at risk of malnutrition
and need a more comprehensive nutritional assessment. See Table 1. for an example of a
screening form used in St Jude Children’s Research Hospital.
Table 1. Nutritional screening for nurses: inpatients done at admission; outpatients

done at diagnosis and every 6 months at St Jude Children's Research Hospital
Are you currently being seen by the clinical nutrition service?

YES/NO
Nutritional Screen
Allergies to food
Weight loss > 5% over 1 month
Weight loss > 2 % over 1 month for infants
Recent unexpected weight gain (please comment)
Nausea/vomiting > 3 days
Nil by mouth or poor oral intake > 3 days
Total parenteral nutrition/tube feedings
Problems or pain with chewing, swallowing, sucking
Modified diet/dietary restrictions (please comment)
Currently being breastfed
Currently taking complementary/alternative medications (please
comment)
Other
Nutritional Consult
No nutritional concerns identified at this time
Nutritional consult requested
Comments
2. Data Collection, Evaluation and Interpretation
In depth nutritional assessment should be provided anytime patients are at risk of

malnutrition. Patients can be identified as at risk by medical personnel, other caregivers, or by
periodic screenings. Unlike nutritional screening, nutritional assessment should be performed
by a professional trained in nutritional assessment, such as a dietitian, trained nurse or a
medical doctor. Nutritional assessment consists of 3 parts: data collection, data evaluation,
and interpretation of findings [20]. Data collection should include diagnosis, historical data,
nutrition-focused physical examination, anthropometry and measures of body composition,
biochemical and hematological indices, and diet [21]. Nutritional assessment is a dynamic
process performed to measure body size and composition for comparison with standards, to
estimate nutritional needs, and to evaluate nutritional status and intake adequacy [22].
Diagnosis
Oncologic diagnoses predispose patients to increased risks for malnutrition. Patients with
cancers of the digestive tract (e.g., esophageal, gastric, pancreatic, liver, gallbladder, bile
duct, and small and large intestine) especially may have severe weight loss due to changes in
normal digestion and absorption [23]. Cancers posing high nutritional risks in children are
advanced/metastatic solid tumors (e.g. neuroblastoma), non-Hodgkin lymphoma (stages III,
IV and relapsed disease), acute myelogenous leukemia (AML), acute lymphoblastic leukemia
(ALL) with poor prognosis (high risk categories and relapsed disease), medulloblastoma and
other brain tumors. All patients undergoing allogeneic HSCT are also at high risk for the
development of malnutrition.
Historical Data
Historical data may include a medical history (acute and chronic illnesses, surgical and
diagnostic procedures and medication use), diet history (use of dietary supplements), oral
intake history, use of alternative or complementary medicine and weight history. Questions
about the psychological status of patients should be asked with special attention to stress and
depression. Patients should be asked about the use of over-the-counter medication, vitamins,
and dietary and herbal supplements.
Nutrition-Focused Physical Examination

The nutrition-focused physical examination of an adolescent and child with cancer is an
integral part of nutritional assessment and should never be omitted. It should include the
general appearance and activity level of the patient.
The clinician should focus on the presence of edema, ascites, cachexia, obesity, skin
changes, dry mucous membranes, petechiae or ecchymoses, healing of wounds, glossitis,
stomatitis, and cheilosis [24].
The physical examination should include an evaluation of body composition, including
fat and muscle stores. Places to assess fat stores are overlying the lower ribs, orbital fat pads,
groins, and armpits. Places to assess muscle stores are temples, clavicles, calves, and
quadriceps (thighs) [25][26]. Other physical signs of malnutrition are liver enlargement and
changes in skin, hair, eyes, face, lymph glands, mouth, teeth, and psychological status
[27][28][29]. Nutritional skin disorders are also common as part of vitamin or mineral
deficiencies [30].
Anthropometry and Measures of Body Composition

These measures can be divided by level of resources needed for accomplishment and by
the need for accuracy and precision as routine, midlevel and advanced. Routine measures
include weight, height/length, head circumference (in children <3 years), weight for
height/length, and body mass index (BMI).
Midlevel measures include triceps skin fold thickness (TSFT), mid-upper arm muscle
circumference (MUAMC), and waist-to-hip ratio. Advanced measures include bioelectrical
methods, dual-energy X ray absorptiometry (DXA), air-displacement plethysmography
(ADP), total body potassium (TBK) counting and isotope dilution methods (deuterium oxide
dilution).
Previous studies have shown that anthropometric measurements such as height, weight
and BMI and their indexes will not accurately identify malnourished patients and should be
used only as a first line of assessment for nutritional problems [31].
It has been shown that, while patients with cancer may have normal weight compared to
healthy controls, they have higher fat mass and lower body cell mass (BCM - the
metabolically active component of fat-free mass), which is an indicator of nutritional status
[31]. Anthropometry can provide a considerable amount of nutritional information about the
patient.
However, it is important to have trained individuals performing the anthropometry to
ensure that the measurements are taken accurately and precisely. Inappropriate measurements
by untrained professionals can provide misleading information on nutritional status.
I. Routine Measures
Weight. Weight should be measured daily while the patient is in the hospital and during
each outpatient visit. Weight can be influenced by the patient’s body composition, fluid
status, medication use, organ enlargement, or tumor mass. Weight should be measured at the
same time of day and similar clothing should be worn for consistency. Weight is not a good
indicator of nutritional status.
Height/Length. Height should be re-assessed in children and adolescents periodically. In
children, height should be reassessed more often during rapid growth and can be affected by
chronic malnutrition (stunting), marginal deficiency of several micronutrients [32] or
impaired growth due to anticancer therapy and steroid use [33].
Head circumference. In children less than 3 years of age, head circumference should be
measured periodically. It is the distance from above the eyebrows and ears and around the
back of the head. It should be compared to past measurements of a child's head circumference
and to normal ranges for a child's sex and age (weeks, months).
Weight for height/length. Weight for height or weight for length is sometimes used in
children, especially in children under 3 years of age, and compared to standards using the
Centers for Disease Control (CDC) growth charts or the World Health Organisation (WHO)
growth charts. Weight for height (W/H) is an indicator of acute malnutrition when a child is
too thin for a given height (wasting) [34]. Height for age (H/A) can be an indicator of chronic
malnutrition. When a child is exposed to inadequate nutrition for a long period of time,
growth is reduced, resulting in stunting [35].
Body mass index (BMI) and BMI z-score. BMI is considered to be a good indicator of fat
mass in adults [36] as well as in children [37] but not a good indicator of BCM [31]. For
calculation of BMI see Table 2.
Table 2. Calculation of body mass index (BMI)
BMI is calculated by dividing the subject's mass (weight) by the square of his
or her height, typically expressed either in metric or U.S. "customary" units:
Metric: BMI = kilograms/meters2
U.S. customary and imperial units: BMI = lb x 703/in2
where lb is the subject's weight in pounds and in is the subject's height in inches
In children, BMI is calculated and compared to z-scores. BMI z-score requires the use of
LMS values (The LMS parameters are the median (M), the generalized coefficient of
variation (S), and the power in the Box-Cox transformation (L)) and a calculation, or it can be
compared to BMI z-score charts. BMI z-score charts can be obtained from the CDC website.
II. Midlevel Measures

Triceps skinfold thickness (TSFT). Arm anthropometry may be useful in assessing fat
stores, especially in children and adolescents with a tumor mass [38][39][40]. In one study,
patients’ skin folds were found to be a poor predictor of fat mass when compared to DXA
[41]. However, in other studies, skinfolds, especially biceps skinfolds, were found to correlate
strongly with the percentage of body fat [37]. They were also found to be easier to obtain in
children than TSFT [37]. Nonetheless, fat stores are not a reliable indicator of malnutrition –
see above.
Fat folds can be used to assess body fat reserves objectively and directly, and should be
re-examined for accuracy. A strict technique should be followed to obtain reproducible
measurements. Calipers are used. TSFT is taken by measuring a fold of skin running parallel
to the length of the arm over the triceps muscle midway between the acromion and olecranon
[8]. Measured values are then compared to reference tables [42][43]. Anthropometric
measures are an inexpensive option for assessing nutritional status, but they can be affected
by fluid retention, dehydration, or steroid therapy [44][45].
Arm circumference. Mid Upper Arm Muscle Circumference (MUAMC) provides a
measure of muscle mass [46]. It is the circumference of the upper arm, measured at the mid-
point between the tip of the shoulder (acromion) and the tip of the elbow (olecranon process).
In children, MUAMC is helpful for the assessment of nutritional status [47] [48]. It is
good at predicting mortality and, in some studies, MUAMC alone [49] or MUAMC for age
[50] predicted death in children better than any other anthropometric indicator. It also
correlates well with lean body mass, as measured by DXA [41].
Calculation of Ideal Body Weight (IBW) and percentage of Ideal Body Weight (%IBW).
For calculation of IBW in children and in adolescents, see Table 3. Patient’s actual weight
should be compared with IBW. Percentage of IBW is typically recorded (see Table 3). The
calculation of weight as a percentage of ideal weight for age, height and gender in children is
shown in Table 3. Percentage of IBW may both under- and over-estimate the severity of
malnutrition in children with a chronic disease [51].
Calculation of weight change. Weight change should be calculated in 1 week, 1 month,
and 6 month intervals.
Table 3. Calculation of ideal body weight (IBW) and percentage of IBW (%IBW)
A. Estimated IBW in children and adolescents

- Option # 1 Used for children under 100cm. in length. Plot weight at the 50th
% ile on the weight for length/height growth curve.
- Option # 2 Plot BMI at 50% ile for age on the BMI for age and gender-
specific growth chart. Multiply by BMI at 50% ile by height in m2
B. Weight as a percentage of ideal body weight:

Express actual weight as percentage of IBW
Option # 1 (actual weight/ideal weight-for-height) x 100
Option # 2 (actual weight/ideal body weight calculated using BMI) x 100
III. Advanced Measures

Bioelectrical Methods. Bioelectrical impedance analysis (BIA) is a method used
commonly for estimating body composition. BIA provides a reliable estimate of total body
water, fat mass (FM) and fat free mass (FFM) under most conditions. It can be a useful
technique for analysis of body composition in healthy individuals and in those with a number
of chronic conditions [52]. The “Tanita” body composition scale has been approved for use in
children. It has been suggested that nutritional assessment of patients with cancer should not
be limited to anthropometric methods, but that body composition analysis should be used as
well [53]. Body composition scales are the most feasible, non-invasive and affordable way to
estimate body composition. The cost is not as high as with other methods for assessing body
composition – see below. However, one disadvantage of BIA is that it usually cannot be used
in children under 5 years of age and requires the patient to be able to stand and hold handles
with both hands.
Dual Energy X-Ray Absorptiometry (DXA). DXA is a non-invasive technique for
measuring bone mineral content (BMC) and bone mineral density (BMD) with minimal
exposure to ionizing radiation [54]. It is also becoming accepted as a standard in clinical
practice for assessing body composition in children [55]. The combination of whole body
BMC, fat mass (FM) and fat-free mass (FFM, very similar to lean body mass) total together
to equal whole body weight. Deficits in bone mineralization are common sequelae of the
treatment of cancer in children and adolescents [56].
Total Body Potassium (TBK) – reference method. Total body potassium (TBK)
concentration is correlated linearly with the size of the BCM. It measures BCM and FFM and
is independent of extra-cellular fluid changes. BCM is the metabolically active component of
FFM and it is the component of FFM that is reduced in malnutrition [57]. The measurement
of BCM has been proposed as the best measurement of nutritional status in populations with
cancer [31], but the technology has not been commercialized (and so is not widely available)
and its interpretation in children with cancer has been criticized [58]. TBK is used mainly as a
reference method due to its cost and time commitment. BCM is calculated from TBK
analysis.
Air-displacement Plethysmography (ADP). ADP is an advanced technique for assessing
body volume, which can then be used to calculate body density and estimate FM and FFM.
The principle is similar to hydrostatic (or "underwater") weighing. The principles of ADP
include densitometry, mass measurement, volume measurement, thoracic gas volume, and
surface area artifact. ADP was found to be the only method that could estimate fat mass
without bias in children [59].
Isotope Dilution Methods (deuterium oxide dilution). Deuterium dilution is used for
measurement of total body water. Deuterium is given orally as deuterium oxide, and after
mixing with body water it is eliminated from the body in urine, saliva, sweat and human milk.
The enrichment of deuterium can be measured by isotope ratio mass spectrometry or Fournier
Transform InfraRed (FTIR) spectrometry.
Biochemical and Hematological Indices

Biochemical data include measures of visceral proteins (albumin, prealbumin, retinol
binding protein and transferrin), blood glucose levels and lipid profiles. Hematological
measures include hemoglobin, hematocrit, and total lymphocyte count. Collected laboratory
values should be compared with reference values.
Visceral proteins. Many factors can affect the level of visceral proteins. C- reactive
protein (CRP) is a measure of systemic inflammatory response. Systemic inflammation is
common in patients with cancer; it disturbs many biochemical indices and has been correlated
adversely with survival [60]. If CRP levels are elevated, visceral protein levels may need to
be adjusted.
Albumin. The normal serum albumin level is 3.5-5 g/dL, and albumin has a half-life of
approximately 20 days. Even though many factors can influence albumin levels, the pre-
operative level of albumin has been found to be an excellent predictor of surgical outcome
[61][62].
A reverse relationship has been found between serum albumin levels and post-operative
morbidity and mortality [63]. When albumin levels are markedly low, it is a common medical
practice to provide albumin infusions. Albumin concentrations can be increased by the use of
corticosteroids, insulin or thyroid hormone and by dehydration (as can other markers).
Albumin concentrations decrease in acutely or chronically ill patients due to the effects of
inflammatory mediators on hepatic protein synthesis [64][65]. Severe liver and renal disease,
malabsorption, intravascular volume overload, and zinc deficiency decrease serum albumin
levels.
Prealbumin and retinol-binding protein. Prealbumin (transthyrretin) and retinol binding
protein, with their short half lives, reflect more recent protein intake rather than an integration
of protein nutritional status. The normal level of prealbumin is 16-40 mg/dL, and prealbumin
has a short half-life of just 2-3 days. It is a favorable marker for acute changes of nutritional
status. Both prealbumin and albumin are acute-phase reactants. A study to determine the
usefulness of visceral proteins in assessing patients after HSCT found that prealbumin,
retinol-binding protein and transferrin all were sensitive markers [66]. Prealbumin, retinol-
binding protein and transferrin have also been shown to be useful for nutritional assessment
of patients in intensive care units [67].
However, prealbumin is influenced by some of the same factors that affect albumin [67].
Therefore, if prealbumin is used as an indicator of nutritional status, it must be recognized
that its concentration can be affected by the inflammatory response and not just by the
nutritional status of the patient [67]. Another factor that affects levels of prealbumin is kidney
failure. In this context, prealbumin levels will be high due to a lack of degradation by the
renal tubules [68]. However, serial prealbumin analysis is also a good predictor of subsequent
albumin levels and adverse outcomes [69].
These tests may be expensive and require drawing blood. A variety of factors can affect
laboratory values, including chemotherapy and other medications, infection, and meals.
Therefore, visceral proteins may not be adequate for assessing nutritional status [70].
Blood glucose levels and lipid profile. In most people, a state of malnutrition indicates
that not enough calories are being consumed to maintain metabolic demands. In malnourished
patients with cancer, increased glucose production occurs in the fasting state, and there are
abnormalities with insulin secretion and action [71]. Malnutrition can cause glucose
intolerance and impairment of insulin secretion [72] [73]. Insulin resistance due to disease or
medication used during treatment, including glucocorticoids and L-asparaginase, is common
[74]. When hyperglycemia occurs, synthesis of very low-density lipoprotein (VLDL) is
driven up, and both serum triglycerides and cholesterol rise.
A lipid profile is a group of tests to measure total cholesterol, high-density lipoprotein
(HDL), low-density lipoprotein (LDL), and triglycerides. In cases of PEM, patients
experience an increase in plasma total triacylglycerol concentration (a measure of fat stored in

the body) and decreased HDL concentration. This is caused by a reduction in the activity of
lipoprotein lipase. Adult patients with cancer have been found to have similar lipid profiles
[75]. One study involving children with cancer showed that those who had undergone HSCT
and those with solid tumors had significantly higher triacylglycerol levels due to increased
VLDL and LDL particles in the blood and significantly lower HDL than healthy children
[76]. L-asparaginase induces prominent changes in the lipid profile, especially
hypertriglyceridemia [77].
Hemoglobin/hematocrit. In a state of malnutrition, hemoglobin and hematocrit levels tend
to decrease due to inadequate amounts of protein consumption and possible iron deficiency.
Other causes of decreased hemoglobin and hematocrit in children with cancer include
chemotherapy, penetration of malignant cells into the bone marrow, radiotherapy,
inflammation, and blood loss [78]. However, hemoglobin and hematocrit levels can be falsely
high if the person is dehydrated. Iron status should be considered when evaluating
hemoglobin and hematocrit, and the best single marker is serum ferritin. However, ferritin is
also an acute phase reactant and hence may be falsely elevated. In this case, measurement of
the transferrin receptor may help establish whether the patient is truly iron deficient [79].
Many children with cancer experience iatrogenic myelosuppression and anemia of sufficient
severity that repeated red blood cell transfusion is required, resulting in some degree of iron
overload rather than iron deficiency.
Lymphocyte count. Malnutrition can be indicated also by a trend of low total lymphocyte
counts, but this may be due to chemotherapy or the impact of the disease [80][81].
Other Studies
Additional studies may be performed to better evaluate a patient’s risk of malnutrition,
including nitrogen balance studies and delayed hypersensitivity testing. Other tests that may
be used to evaluate patients’ nutritional status are the prognostic nutritional index and the
creatinine height index, that is a measurement of the 24-hour urinary excretion of creatinine,
which is related to the patient’s muscle mass and can be used as an indicator of malnutrition
[58]. Tests for maldigestion and malabsorption may be required in some instances.
Following the screening assessment, the choice of tests and the timing of their
performance will be dictated by the particular clinical circumstances.
I. Nitrogen Balance
Nitrogen balance studies provide assessments of protein metabolism in the body, but
these are not used commonly as a clinical tool due to the necessity of urine collection.
Nitrogen balance occurs when nitrogen output equals nitrogen input. Negative nitrogen
balance indicates inadequate protein intake, and positive nitrogen balance indicates nitrogen
retention [82]. In patients with cancer, negative nitrogen balance is a result of inadequate
intake of protein and/or increased protein catabolism. Continued negative nitrogen balance
can lead to protein malnutrition, which is a cause for concern in patients undergoing
anticancer treatment [83]. Patients’ nitrogen balance can improve with the use of high-
nitrogen total parenteral nutrition [84][83][85]. It is important to monitor nitrogen balance to
prevent deterioration of lean body mass and to ensure quicker recovery. Measurement of total
nitrogen is not usually available, but a reasonable surrogate is to monitor 24h urinary urea
excretion and to determine how it responds to an increase in protein intake. Nitrogen intake is
measured by dividing grams of protein consumed by 6.25, as it is estimated that 6.25 grams
of protein contain 1 gram of nitrogen. Urine collected for 24 hours over 3 consecutive days is
the ideal way to estimate nitrogen output [86]. Such collections are challenging in small
children, especially those wearing diapers, due to difficulty in achieving complete samples.
II. Delayed Hypersensitivity Testing

Delayed cutaneous hypersensitivity (DCH) is a test to determine whether the body reacts
to foreign substances such as antigens or allergens that are injected into the skin. A reaction
should occur 24-48 hours after exposure to the foreign substance. This type of test measures
cell-mediated immunity. It was developed for use in adult patients and requires prior exposure
to an antigen; therefore it is less useful in infants and young children.
Malnutrition can affect the levels of circulating antibodies that respond to the stimuli or
prevent the cells that regulate immunity from recognizing foreign stimuli, giving a person a
false negative response in DCH [87].
As a result, an improvement in nutritional status should increase DCH. In one study
involving 160 patients with cancer who were undergoing surgery, chemotherapy, radiation, or
supportive care, nutritional repletion through intravenous hyperalimentation (IVH) was
provided, and skin tests before and after IVH were examined [88].
The study showed that patients with nutritional repletion either remained positive or
converted from negative to positive. This test is not commonly administered in pediatric
clinical settings.
III. Prognostic Nutritional Nutritional Index

Prognostic nutritional index (PNI) is a method to determine nutritional status and risk of
complications. PNI involves using a formula that can include variables such as albumin,
prealbumin, delayed hypersensitivity, transferrin, and TSFT. This test has not been validated
for infants and children.
A similar test, the simple pediatric nutritional risk score, was found to be suitable for
routine use to identify patients at risk of malnutrition during hospitalization. The test includes
assessment of dietary intake, diarrhea and vomiting, pain, and the ability of the patient to eat
[89]. The simple pediatric nutrition risk score has not been tested for children undergoing
anti-cancer treatment.
IV. Creatinine Height Index

The creatinine height index (CHI) is a method to assess relative muscle mass. Creatinine
is excreted in the urine and is a derivative of creatine, a storage form of protein in muscle.
When an increased breakdown of muscle occurs in the body, the loss of creatinine is seen in
the urine. The CHI can be used to assess children’s muscle mass and determine whether they
are protein malnourished and need protein repletion in the diet.
The CHI is defined for children as the ratio of 24-hour creatinine excretion by the patient
to the amount of excretion of a healthy child of similar height. Age is not considered. If the
CHI is close to 1.0, the child is within the normal range. If it is closer to zero, the child may
be protein-malnourished and need nutritional supplementation [90]. One study used CHI as a
way to identify a patient population as malnourished or well-nourished before surgery and to
determine whether there was a difference in post-operative complications [91].
V. Maldigestion and Malabsorption

Maldigestion or malabsorption may be assessed by a 3-day fecal fat test and calculation
of the percentage of dietary fat absorbed (3-day stool collection combined with 3-day dietary
record). Coefficient of fat absorption values are < 85% for infants and < 93% for older
subjects, and can be used to define steatorrhea [92]. Maldigestion can be due to loss of
regulated gastric emptying, insufficient pancreatic exocrine function, bile salt deficiency, or
intestinal mucosal disease. Malabsorption can be caused by loss of intestinal surface area,
impaired circulation or lymphatic damage in the gut, mucosal infiltration with abnormal cells,
genetic mutations of transport proteins, or impaired gut motility.
Diet
Evaluation of a patient’s diet is an important part of nutritional assessment and consists of
3 parts: evaluation of a dietary history, assessment of current dietary intake and comparison
of dietary intake to estimated calorie needs.
I. Dietary History
Dietary history consists of information about current dietary orders, prior history (current
home feeding regimen, food consumption patterns, quality and quantity of food, food
preferences, feeding environment, and food allergies and intolerances), social issues
(socioeconomic status, caregivers’ perception of the patient’s nutritional status, and religious
or cultural factors that affect food intake), and clinical factors (vitamin and supplement use,
stool habits and characteristics, activity level, developmental status, and sleep patterns) [93].
II. Dietary Intake

Oral intake can be assessed using different methods. Some common methods are 24-hour
dietary recall (asking about all oral intakes from the previous day), a 3-day calorie count, or a
food frequency questionnaire [94].. Obtaining a patient’s food history is an inexpensive way
to determine his or her current eating habits. However, it requires the patient or caregiver to
be able to recall what the child eats and estimate portion sizes.
III. Comparison of Dietary Intake to Estimated Calorie Needs

Current dietary intake will be compared with estimated caloric needs. A patient is
considered at nutritional risk if he or she consumes less than 50% of estimated caloric needs
for up to 3 days [95] or less than 80% for more than 3 days [96] .
3. Nutritional Risk
Weight and height or length and BMI, or weight for height in children younger than 3
years, should be compared with values on age- and sex-specific growth charts. For children
living in the United States, CDC growth charts should be used [97][98]. CDC charts have a
higher percentage of children under the age of 2 being at risk for malnutrition. The CDC
charts were formulated using a broader, more diversified sample of children than the NCHS
and Tanner-Whitehouse charts [99]. For children from other countries, WHO charts should be
used for children up to age five, since these charts only extend to this age, beyond which the
CDC charts should be used [100]. The WHO created a growth chart using children from
ethnicities and cultures from various parts of the world [101].
Studies have shown that infants who are breast-fed exclusively grow at a different rate
than formula-fed infants; therefore, WHO charts specific to breastfed children should be used
for those infants [102]. Fenton charts are used for pre-term infants. These charts plot pre-term
infants from 24 to 50 weeks of gestation and are not sex-specific. Specialized growth charts
are also available for children with Down syndrome, cerebral palsy, Turner syndrome,
Prader-Willi syndrome, and achondroplasia.
Nutritional intervention is indicated for children at risk [96]. Determination of nutritional
risk is illustrated in Table 4.
Table 4. Nutritional risk
Screening – periodically
Assessment – at diagnosis and depending on the screening values
ESTIMATION of RISK
Anthropometric Measurements
Weight loss
 More than the 5% weight loss in 1 month
 Current percentile weight or height fallen by 2 channels or more
Weight for Age
 Less than the 5th or >85th percentile
Length or Height for Age
 Less than the 5th percentile height-for-age (may indicate chronic malnutrition)
Weight for Length or Height
 Less than the 5th percentile or >95th percentile weight-for-length (under 3 years)
 Less than the 5th percentile - underweight (indicator of inadequate weight gain)
 More than the 95th percentile - indicator of obesity
Body Mass Index (BMI)
 More than the 95th percentile - obese

 More than the 85th percentile - overweight
 Less than the 15th percentile - undernourished
 Less than the 5th percentile - severely undernourished
Ideal Body Weight (IBW) calculated from weight for length/height
 More than110% - overweight

 85-89% - mild undernutrition
 More than 75-84% - moderate undernutrition
 Less than 75% - severe undernutrition
Ideal Body Weight (IBW) calculated from BMI
 More than120% - overweight

 80-89% - mild undernutrition
 70-79% - moderate undernutrition
 Less than 70% - severe undernutrition
Head circumference-for-age
 More than the 95th percentile (may indicate macrocephaly)

 Less than 5th percentile (may indicate microcephaly or chronic malnutrition during
fetal life or early childhood)
Arm anthropometry
Assessment of subcutaneous fat and muscle mass for signs of under/overweight
 Triceps skin fold estimation of energy stores - compare to reference values

 Mid-upper arm muscle circumference (MUAMC), indicator of lean body mass –
compare to reference values
Nutrient intake
Less than 50% of estimated energy needs for up to 3 days

Less than 80% of estimated energy needs for a longer period of time
C. Common Complications of Treatment

Affecting Nutrition
Patients undergoing chemotherapy, radiation and HSCT can experience any or all of the
following side effects: nausea, vomiting, mucositis, constipation, diarrhea, altered taste, loss
of appetite, pancreatitis, colitis and pneumatosis intestinalis.
Any of these side effects could result in undesirable weight loss, PEM or cancer cachexia.
In addition, HSCT patients are at risk for GVHD and veno-occlusive disease (VOD).
Protein Energy Malnutrition
PEM occurring in association with cancer is usually a mixture of inadequate intake

combined with the stress and catabolism caused by the disease, and adverse side effects of the
treatment. An inadequate energy intake is associated with loss of adipose tissue which can be
measured as a reduction in skin fold thicknesses (see anthropometric measures). It is useful to
think of PEM as adapted or unadapted [20].
The central concern is whether the subject’s protein homeostasis is able to adapt to an
insufficient intake; if so the serum albumin will remain normal. In the unadapted state, protein
homeostasis is unable to adapt; serum albumin falls and there is rapid wasting of muscle mass
as occurs in cancer cachexia. Most often there are differing degrees of energy and protein
insufficiency. Hence the use of the term PEM, which was first introduced to describe
malnutrition occurring in children.
Cancer Cachexia
Cancer cachexia is a well recognized condition in which there is rapid deterioration in

body composition. Wasting occurs in skeletal muscle as well as other components of lean
body mass (see anthropometric measurements of muscle wasting).
Furthermore, there is a disturbance of whole protein homeostasis with net catabolism,
negative nitrogen balance, a decrease in blood urea nitrogen and a fall in serum albumin.
If untreated, cancer cachexia results in rapid deterioration of the patient’s nutritional
status, leading to a “nitrogen death”. In children and adolescents with cancer, cachexia is
influenced by several factors, including type of disease, socioeconomic status, and type of
treatment.
Graft-versus-Host Disease
GVHD is a potential complication following allogeneic HSCT. The donor's

immunoregulatory cells attack the patient's organs, impairing their ability to function and
increasing their susceptibility to infection. To increase the odds of engraftment and minimize
the risk of GVHD, the donor and patient are matched as closely as possible based on human
leukocyte antigen typing. There are two types of GVHD: acute and chronic. Traditionally, the
presence of GVHD beyond 100 days after HSCT was called chronic GVHD. However, the
National Institutes of Health recommends now that acute and chronic GVHD should be
distinguished by clinical manifestations and not by time after transplantation.
The new classification includes late-onset acute GVHD (after 100 days) and an overlap
syndrome with features of both acute and chronic GVHD [103]. Acute GVHD. The signs of
acute GVHD may be a skin rash appearing on the individual's hands and feet. Cramping,
nausea, and watery or bloody diarrhea are other signs of GVHD in the stomach or intestines.
A rising bilirubin with jaundice may be a sign that acute GVHD has affected the liver.
Chronic GVHD can be multisystemic involving the skin, gastrointestinal tract, liver,
musculoskeletal system, and the immune system. To date, there has been no effective means
to prevent chronic GVHD. The most successful treatment of patients with chronic GVHD is a
systematic approach to management with a multidisciplinary team. Two means of treating

GVHD that have been found effective are extracorporeal photopheresis and psoralen and
ultraviolet A irradiation (PUVA) therapy.
Extracorporeal photopheresis involves removing the blood from the body and then
treating it with a combination of ultraviolet light and certain drugs that become active on
exposure to light. Once the blood has been treated, it is then returned to the patient. PUVA
therapy is a photodynamic therapy that is used to treat GVHD specifically affecting the skin.
During PUVA therapy, the patient will receive the drug psoralen, which becomes activated in
the presence of light, either by mouth or by applying it to the skin. The patient then undergoes
ultraviolet A radiation.
If an individual develops GVHD, he or she can experience any or all of the following
side effects: dry mouth, decreased secretion of saliva making swallowing difficult, and
difficulty eating acidic foods because of burning and discomfort. GVHD may also cause a
lack of lubrication in glands in the stomach and intestines, which interferes with the ability to
properly absorb nutrients from food. Other symptoms may include heartburn, stomach pain,
nausea, diarrhea and vomiting. There may be malabsorption of macronutrients from food and
weight loss. Patients with GVHD often require immunosuppressive medications such as
cyclosporine, mycophenolate, and steroids. Dietary guidelines are to follow a low-bacteria,
lactose-free, and/or GVHD low residue, bland diet.
Veno-Occlusive Disease
Veno-occlusive disease (VOD) is a potentially serious liver problem caused by high

doses of chemotherapy or radiation given before HSCT. The blood vessels within the liver
become swollen or obstructed, impairing the liver's ability to remove toxins, drugs, and waste
products from the bloodstream. Fluid accumulates in the liver, causing swelling and
tenderness. A patient with VOD may experience any or all of the following symptoms:
jaundice, enlarged liver, pain and tenderness in the area of the liver, rapid weight gain, edema,
or accumulation of fluid in the abdominal cavity (ascites) The nutritional intervention for
VOD is to limit fluid intake to maintenance level or less. These patients may require
aggressive fluid restriction to prevent a buildup of fluid that may cause respiratory and renal
complications. This may compromise energy intake for a short time. Parenteral nutrition is
usually concentrated to the limit to provide maximal energy with restricted volume. The
features of VOD are encountered usually in the first 4 weeks after the
conditioning/preparative regimen for HSCT. VOD is also referred to as sinusoidal obstruction
syndrome (SOS) specifically for cases resulting from chemotherapy or HSCT.
Renal Complications
Patients may have pre-existing renal dysfunction as a result of their underlying disease
and/or previous therapy. High dose chemotherapy and radiation as part of anti-cancer
treatment or administered in the preparative regimen for HSCT may cause renal damage
directly.
Rapid cytolysis of tumor can cause tumor lysis syndrome with renal injury resulting from
hyperphosphatemia. Post-transplant infections can lead to acute renal dysfunction because
these may be accompanied by hypotension and renal hypoperfusion.
Antimicrobials used for prophylaxis and treatment of infections are also commonly
nephrotoxic. A patient with renal dysfunction may require reduced volumes of fluid,
decreased amounts of protein or amino acids, or adjustment in electrolytes. During renal
dysfunction, parenteral nutrition is usually concentrated to the limit to provide maximal
energy with restricted volume.
Mucositis
Mucositis is a common occurrence in cancer patients. It is a painful inflammation and

ulceration of the mucous membranes lining the digestive tract and occurs due to
chemotherapy, local radiation, and total body irradiation. It also reduces an individual’s
ability to eat and drink adequately.
Pain medications can help manage mucositis, but intravenous infusions may also be
necessary to prevent dehydration and malnutrition. Furthermore, oral glutamine
supplementation has been shown to decrease the severity of mucositis in children undergoing
HSCT [104].
Infection
The risk of bacterial, viral, and fungal infections is high in cancer patients, as treatment
destroys the normal production of neutrophils, monocytes, and macrophages. Common side
effects of infection include diarrhea, nausea and vomiting. Food safety guidelines are
recommended during periods of neutropenia. Typically, a low bacteria diet may be indicated.
Furthermore, if the patient is symptomatic, a low lactose diet may be needed due to a decrease
of intestinal lactase from antibiotic medication. Probiotics, such as Lactobacillus, may also be
administered to modify the enteric flora. However, more research is needed to confirm safety
and efficacy of probiotics on the immune system in neutropenic patients [105].
Pancreatic Insufficiency
Pancreatic insufficiency occurs when the pancreas does not secrete enough digestive
enzymes for normal digestion to occur. It may be caused by high doses of chemotherapy or
radiation. In severe cases, malabsoprtion may occur. This leads to deficiencies of essential
nutrients and is associated with loose and fatty stools (steatorrhea). The coefficient of fat
absorption values are < 85% for infants and < 93% for older subjects, and can be used to
define steatorrhea [91]. An easier and more effective method for determining maldigestion
and malabsorption resulting from pancreatic insufficiency is a fecal elastase test. This test is a
much more sensitive method of determining pancreatic insufficiency and the need for
pancreatic enzyme replacement therapy than a fecal fat test.
Hemorrhagic Cystitis
Hemorrhagic cystitis is diffuse inflammation of the bladder leading to dysuria and

hematuria. It occurs in patients undergoing HSCT due to the conditioning regimen of
chemotherapy (especially if this includes cyclophosphamide), radiation or infection. Fluid
intake and output needs to be monitored closely in patients with hemorrhagic cystitis. Fluid
intake may need to be increased.
D. Nutritional Requirements
Different methods exist for estimation of calorie and protein needs; for example,
calculation of calorie needs in children undergoing HSCT (Table 5), using indirect
calorimetry, or using double labeled water, the “gold standard” of caloric and protein
estimations. Resting metabolic rate should be calculated using the FAO/WHO/UNU Expert
Consultation for Human Energy requirements [106] and adding the activity quotient.
Table 5. Energy requirements (kcal) of pediatric HSCT patients
Age Calories (kcal)

1-12 months BMR1 x 1.6-1.8
1-6 years BMR x 1.6-1.8
7-10 years BMR x 1.4-1.6
11-14 years BMR x 1.4-1.6
15-18 years BMR x 1.5-1.6
>19 years BEE2 x 1.5
1
BMR equations: WHO Method [143] located under the Calculators tab.
2
BEE equations: Harris-Benedict Equation [117]
Indirect Calorimetry
Indirect calorimetry can be useful anytime hypermetabolism or hypometabolism is

suspected and precise calorie requirements need to be estimated for weight management. The
energy needs of a patient can be estimated either by using the World Health
Organisation(WHO) predictive equation [106] or measured directly by respiratory gas
exchange using an indirect calorimeter. Indirect calorimetry by the metabolic cart test or
portable resting metabolic rate analyser measures energy expenditure and determines the
caloric needs of the patient. Indirect calorimetry measures oxygen consumption, carbon
dioxide production, and the respiratory quotient to determine energy expenditure and caloric
needs. It is useful to relate the measured resting metabolic rate (RMR) with the calculated
RMR [107].
Double Labeled Water
Double labeled water is considered the “gold standard” for measuring metabolic rate. It is
a form of water in which both the natural hydrogen and oxygen moieties have been replaced
partly or completely for tracing purposes (i.e., labeled) with an isotope of each element.
An average metabolic rate is measured over a period of time. The minimum number of
samples is two; the initial sample and the second sample taken later. This method is safe for
infants, children and adolescents. However, one disadvantage is its high cost.
Energy Needs
The energy needs of children with cancer are not well described. On the one hand, energy
requirements may be higher due to mucositis, nausea and vomiting, and diarrhea.
Furthermore, GVHD may also increase energy requirements after transplantation.
However, a study by Ringwald-Smith et al [95] showed that the standard estimation
equations for energy expenditure overestimate the energy needs of pediatric patients
undergoing HSCT significantly.
Similarly, a study on children undergoing allogeneic HSCT showed significant
reductions in Resting Energy Expenditure (REE) after transplantation [108]. Until more
research is undertaken on estimating energy needs, the use of indirect calorimetry is the best
method currently available.
Energy needs may be increased because of treatment, fever, infection, GVHD, metabolic
complications, and the normal growth demands of children. Protein needs are increased for
tissue repair and to decrease breakdown of lean body mass. These may be increased during
high-dose corticosteroid therapy and during active GVHD, and may be modified if hepatic,
renal, or neurological function is altered.
Fat needs are altered when lipid clearance is decreased in patients with hepatic
dysfunction Carbohydrate needs may be decreased if hyperglycemia occurs. For obese cancer
patients, use adjusted body weight to calculate energy needs. See Table 6 for identifying
failure to thrive (FTT) and calculating the energy requirements in this circumstance.
Table 6. Calculating failure to thrive (FTT)
1) Weight for height/length below 5th percentile

2) Less than 80% of IBW based on height
FTT (kcal/kg) = (RDA kcal for weight for age) x IBW (weight for height at 50%)/
actual weight
OR add on 10% energy factor, using the BMR.
Protein Requirements
Children undergoing anticancer treatment have been shown to have decreased lean body
mass [108]. Therefore, protein requirements should be increased to minimize this loss.
Protein is often calculated per 1 g nitrogen. In patients receiving parenteral nutrition, the usual
non-protein calories to nitrogen (NPC: N2) ratio is 150 to 250 NPC for every gram of nitrogen
provided.
When monitoring for response, assess the prealbumin levels weekly. Prealbumin is
influenced by fluid disturbances as well as renal and hepatic failure; therefore, prealbumin
concentrations should not be used as a measure of response in those patients who are
hemodynamically unstable. A baseline prealbumin should be obtained at the beginning of
enteral or parenteral therapy.
Albumin has a long half-life and therefore should not be used to assess response to
nutritional support over a short period of time. See Table 7. for the equation to calculate
protein requirements, Table 8 for the special circumstance of HSCT and Table 9 for the
equation to determine protein requirements for those with FTT.
Protein restriction may be required in patients with renal failure and liver failure.
Table 7. Calculating protein requirements: (The equation to determine the grams

of protein/kilogram of body weight of a patient)
(Total energy / NPC) x 6.25

Body weight
NPC = nonprotein calories
NPC for low-stress patients (1 g nitrogen / 250 kcal)
NPC for medium-stress patients (1 g nitrogen / 200 kcal)
NPC for a catabolic child (1 g nitrogen / 150 kcal)
1 g nitrogen = 6.25 g protein
Table 8. Protein requirements (g/kg/d) of pediatric HSCT patients
Age Protein (g/kg/d)

1-12 months 3
1-6 years 2.5-3
7-10 years 2.4
11-14 years 2
15-18 years 1.8
>19 years 1.5
Table 9. The equation to determine protein requirements for those with FTT
Protein = [protein required for weight for age (gm/kg/d) x IBW (kg)]/3.5
For patients with a pre-renal elevation of blood urea nitrogen (BUN) not related to renal
failure (eg, gastrointestinal bleed, aggressive therapy with loop diuretics), protein restriction
should be considered if the BUN rises above 60 (mg/dL). Also, it should be taken into
consideration if the patient is maintained on catabolic steroid therapy. For Failure to Thrive
(FTT), protein should be increased to 1.5 to 2.0 times the DRI (Dietary Reference Intake) for
age. Avoid exceeding 4 g/kg. In a patient receiving total parenteral nutrition, use the total
energy: nitrogen ratio of 150 to 250 NPC for every gram of nitrogen provided. Protein
tolerance can be monitored with BUN, serum creatinine, nitrogen balance, visceral proteins,
and ammonia levels in patients with liver failure.
Fat Requirements
For infants and toddlers, fat intake equivalent to 30% to 55% of total energy is
appropriate. Those older than 2 years may need less than 30% without compromising growth.
More than 50% is not recommended. In total parenteral nutrition, fat should supply 20% to
60% of energy needs. Upper limit in infants is 4 g/kg/d. Medium-chain triglyceride (MCT) oil
does not provide essential fatty acids (EFA) nor facilitate absorption of fat soluble vitamins.
Monitor the patient receiving more than 86% of total fat as MCT oil, which contains 8.3
kcal/g. Microlipid is a source of EFA, containing 4.5 kcal/mL.
Fluid Requirements
Monitoring for fluid tolerance and response. Fluid needs may be increased in patients
with significant losses like those with gastrointestinal (GI) suctioning, GI fistulas, persistent
vomiting, diarrhea, and high fever. Fluid needs may be decreased in patients with renal failure
or pulmonary edema, patients at risk for VOD, or patients at risk for capillary leak syndrome,
which includes those undergoing high-dose chemotherapy, total body irradiation, and
interleukin therapy.
Table 10. Calculating fluid needs
Method 1
Maintenance Body Weight (kg) Amount per Day
1-2 120-150 mL/kg
3-10 100 mL/kg
11-20 1,000 mL + 50 mL/kg for each
kg above 10
>20 - 40 1,500 mL + 25 mL/kg for each
kg above 20
>40 1,500 mL/m2 body surface area
Method 2
Maintenance: > 11 kg = 1,500-1,800 mL/m2/day
Fluid tolerance and response can be monitored by assessing weight changes, 24-hour
fluid input and output, BUN, physical examination including skin turgor, and urine output.
See Table 10 for calculating fluid needs.
Vitamin and Mineral Needs
Vitamins and minerals are essential for normal growth and development in children.
While there are no specific requirements for children with cancer, the patient’s nutritional
plan should meet 100% of the Dietary Reference Intake (DRI) of vitamin and minerals. Risk
of vitamin deficiency is higher in patients with diarrhea, vomiting and malabsorption. If
vitamin and mineral supplementation is required, iron-free supplements are generally
recommended as many patients experience repeated red blood cell transfusion, resulting in
some degree of iron overload rather than iron deficiency. Of particular importance in children
undergoing treatment for cancer are the nutrients required for bone development and
maintenance. A recent study showed that vitamin D insufficiency and deficiency are common
in children after anticancer treatment [109]. Vitamin D deficiency can be caused by many
things, including limited sun exposure and malabsorption. Furthermore, long-term survivors
are at risk for loss of bone mineral density (BMD) and subsequent osteoporosis [110].
Therefore, vitamin D and calcium levels should be monitored. The latest recommendations
for Vitamin D intake are 600 IU/d [111]. Patients undergoing treatment may also be at risk
for other vitamin and mineral deficiencies, especially vitamin K, zinc, copper and selenium.
More research is needed regarding vitamin and mineral supplementation during treatment.
E. Nutritional Therapy
The goals of nutritional therapy for patients undergoing anticancer treatment are to
maintain weight, and to achieve age-appropriate growth and weight gain after treatment.
These goals can be achieved by dietary modifications, use of dietary supplements,
appetite stimulants, or nutritional support.
Oral Intake
An evaluation of dietary intake and adequacy during anticancer treatment is paramount.

Understanding how well the patient is eating before and during treatment will provide
invaluable information that will aid in assessing the individual’s nutritional status and
developing a nutritional plan. Detailed food records can be used to determine food
preferences and aversions, and assist in managing the individual’s nutritional care. A
complete dietary history should include an evaluation of oral and gastrointestinal symptoms
related to chewing and swallowing, dental health, taste alterations, heartburn or gastric reflux,
mucositis, and bowel habits.
Appetite Stimulants
The use of appetite stimulants in this patient population is recommended when other
attempts to increase oral intake (such as oral supplements) have failed. A variety of appetite
stimulants exists (see Table 11 ).
Table 11. Appetite stimulants
Trade
Agent Adverse Reactions
Name
Drowsiness, dizziness, depression,
detachment, anxiety, difficulty concentrating,
Dronabinol Marinol
mood change, xerostomia, orthostatic
hypotension, tachycardia, ataxia, headache
Edema, insomnia, fever, headache,
depression, breakthrough bleeding and
Megestrol amenorrhea, changes in menstrual flow,
Megace
acetate nausea, vomiting, stomach cramps, cholestatic
jaundice, hepatotoxicity, thrombophlebitis,
hyperpnea
Drowsiness, headache, fatigue, thickening of
bronchial secretions, pharyngitis, nausea,
Cyproheptadine Periactin
diarrhea, abdominal pain, xerostomia,
arthralgia
Nutritional Support
There are two main types of nutritional support available – enteral nutrition (EN) and
parenteral nutrition (PN), depending on whether the gastro-intestinal tract is used for the
delivery of support. Delivery of nutrients into the gut is the preferred method of feeding when
use of the gastrointestinal (GI) tract is feasible. Utilization of the GI tract may not be feasible
for the following reasons: persistent vomiting, intractable diarrhea, GVHD of the gut, ileus, a
prolonged period of bowel rest after surgery, and inadequate gag reflex. Parenteral nutrition
should only be utilized when the GI tract is not usable for at least 7 to 10 days. Exceptions to
the “7- to 10-day rule” are children younger than 4 years of age or those who are already
malnourished. There are different options for administration of EN. For example, gastrostomy
or jejunostomy; nasogastric, nasojejunal, orogastric and orojejunal tubes. Enteral feedings
using gastric or post-pyloric tubes are a viable option for some groups of patients, including
those undergoing HSCT. Nasojejunal (NJ) tubes were used successfully in one small pilot
study of adult allogeneic transplant recipients [112]. Mixed success has been achieved in
other studies using naso-gastric (NG) tubes in adults and children [113][114] [115].
Difficulties with successful enteral feeding are related primarily to feeding intolerance with
nausea, vomiting, and diarrhea. There has also been reluctance among care providers to insert
tubes into neutropenic and/or pancytopenic patients, although the risk of infection has not
been proven to be greater than the risk of feeding parenterally throughout transplantation.
Parenteral nutrition (PN) is not always superior to individualized enteral feeding. It is
recommended that total PN (TPN) be reserved for patients who cannot take advantage of
enteral feedings (EN). Studies have found that, although TPN is shown to preserve body mass
in critically ill patients, it is also linked to specific complications and high costs [116].
Although EN has been found in some cases to be less effective in maintaining BCM, use of
EN did not change the outcomes of hematological recovery, length of hospitalization, and
survival. However, with EN, the most common toxicities and the high costs that are
associated with TPN were avoided [113]. Studies have also found that an aggressive enteral
feeding program, along with the help of a supportive team, can help to maintain nutritional
status in the pediatric oncology population. A study by Hastings, White, and Young [117]
found that EN via a NG tube was effective in providing nutrition during HSCT. Their
findings were supported by a study that found that EN, when tolerated, was successful in
limiting nutritional decline during HSCT [114]. A study by Stratton and colleagues [118]
looked specifically at enteral and parenteral nutrition (PN) tube feeds with respect to appetite
sensations and food intake. This study found that EN improved anorexia and voluntary food
consumption typically in malnourished patients during recovery and that “small amounts of
food taken orally during PN may relieve appetite sensations more effectively than PN alone.”
The study concluded that total energy intake is amplified when PN is combined with oral
food intake. PN has also been shown to delay resumption of oral intake in HSCT patients
[119]. A study by Papadopoulou and colleagues [114] examined EN specifically after HSCT.
Their research found that patients receiving EN had fewer episodes of fever, as well as fewer
positive blood cultures. The study also observed that EN is more effective in preventing
deterioration of nutritional status after HSCT than in patients not receiving EN. A significant
positive correlation between duration of feeds and improvement in nutritional status was also
found. EN provides an easy way to administer oral medications, with the exception of
cyclosporine, given via a NG tube. A lower incidence of diarrhea was also found in patients
on EN in comparison to those on TPN [115]. One study found that, during a time of extreme
gut toxicity, continuous NG feeding could accelerate the healing process [120]. Other studies
concerning EN and TPN found that EN maintained mucosal integrity by supporting the
barrier function of the gut and therefore lowering the risk of bacterial translocation
[121][122].
Glutamine
The amino acid glutamine has been highlighted as a fuel source for rapidly replicating
cells. Several studies have attempted to evaluate the clinical efficacy of glutamine-
supplemented nutrition in patients with cancer [123]. Although one randomized, controlled
study of glutamine-supplemented parenteral nutrition showed improved nitrogen balance,
fewer clinical infections, and shorter length of hospital stay [124], subsequent studies have
demonstrated similar but less dramatic results in allogeneic [125] and autologous [126] HSCT
recipients. Another study using parenteral glutamine supplementation during autologous
HSCT was associated with more relapses and death [127]. Studies using oral glutamine
supplementation have found that they have no significant effects on clinical outcomes during
HSCT [128][129]; therefore, the routine use of glutamine has not yet been justified. However,
other studies suggest that glutamine supplements are safe and effective in reducing the
severity of mucositis in children undergoing anticancer treatment and should be given
consideration in the routine care of patients with cancer [104]. Patients with glutamine-
supplemented diets have shown a significant decrease in the number of days they required
morphine and total parenteral nutrition (TPN), both of which are objective indicators of a
decrease in the severity of mucositis [130].
Refeeding Syndrome
Refeeding syndrome is a problem that often occurs with the initiation of aggressive
nutritional support. PN support is most commonly associated with the onset of refeeding
syndrome, but this metabolic abnormality has been found to occur with both EN and PN. This
syndrome is characterized by the individual becoming metabolically unstable with the
development of hyperglycemia, hyperlipidemia, and hypophosphatemia. Individuals at
highest risk for developing refeeding syndrome include chronically semi-starved, marasmic
patients who have adapted largely to the use of free fatty acids and ketone bodies as energy
sources. Some patients undergoing anti-cancer treatment may fit into this category because of
treatment-induced weight loss and anorexia. Because nutritional support is commonly used
with the HSCT population, a clear understanding of the causes and ways to prevent refeeding
syndrome is crucial. To avoid the development of refeeding syndrome, nutritional support in
patients at risk should be increased slowly [131][132].
Different Diets used in Children with Cancer
Food poisoning can occur if a person eats or drinks something that contains harmful
germs. Food consumed by immunocompromised patients should be prepared in a manner to
minimize bacterial growth. Table 12. lists recommended dietary practices for
immunocompromised patients. Some hospitals use stricter guidelines than those listed.
Although there has been little convincing evidence that a low-microbial meal plan leads to a
better outcome in the oncology setting, it is clear that food pathogens exist and, intuitively,
fewer pathogens should reduce risk. A reasonable approach to keep recommendations current
and appropriate is to consider questionable items individually with systematic analysis of
food culture data. Because food culturing may be impractical for many institutions, another
way to obtain food safety information is from reputable sources.
Table 12. Dietary practices for immunocompromised patients
 Practice good hand washing before, during, and after preparing and eating meals.
 Do not share food with others.
 Avoid foods from street vendors, salad bars, and shared bins of foods in grocery
stores.
 Wash raw foods well before eating; inspect for bruises, cuts, and mold. Do not eat
food that smells bad.
 Cook meats, fish, poultry, and eggs until well done.
 Do not eat hot dogs, luncheon meats, or deli meats, unless these are reheated until
steaming hot.
 Do not eat pates or meat spreads unless canned or shelf stable.
 Avoid unpasteurized selections of dairy products, fruit juices, vegetable juice, honey,
and beer.
 Do not eat soft cheeses such as feta, brie, and camembert, blue-veined cheeses, or
Mexican-style cheeses such as queso blanco, queso fresco, and panela, unless these
have been cooked. Pasteurized cheeses are still considered high risk.
 Avoid raw eggs and smoked or pickled fish.
 Keep foods at lower than 40°F or greater than 140°F to minimize growth of bacteria.
 Clean all preparation items thoroughly before and after use to avoid cross-
contamination.
 Keep refrigerated leftovers for no more than 3 days.
 Well water should come from a well that is tested yearly and it should be boiled 15 to
20 minutes before use.
 Use clean utensils and food-preparation areas.
 Divide leftovers into small units and store in shallow containers for quick cooking.
 Refrigerate leftovers within 2 hours of cooking.
 Discard leftovers that were kept at room temperature for more than 2 hours.
 Reheat leftovers or heat partially cooked foods to more than 165°F throughout before
serving.
 Bring leftover soups, sauces, and gravies to a rolling boil before serving.
F. Nutritional Monitoring and Evaluation

Nutritional monitoring and frequency of reassessment will depend on the risk level and
condition of the patient [95]. Patients at high risk will be assessed within 24 hours of
admission and reassessed at a minimum of 2 times per week. The following factors, among
others, may be true of these high-risk patients:
 On nutritional support
 Bone marrow transplantation (initial – see Table 13)
 Weight loss of 3% to 5% in the last month
 Nil by mouth status greater than 3 days
Patients at moderate risk will be assessed within 72 hours of admission and reassessed, at
a minimum, one time per week. These patients may present the following features, among
others:
 Non-chemotherapy induced nausea, vomiting and diarrhea

 Mucositis and other oral problems
 Modified diet
Patients at low risk will be assessed within 72 hours of admission and reassessed as
indicated. It is possible that these patients may be newly diagnosed and on protocols. Table
13 shows a suggested schedule for monitoring indices during early stages of HSCT.
Table 13. Suggested schedule for monitoring blood biochemical and other indices during
early stages of HSCT
Test Frequency
Sodium, potassium, chloride, Every day until stable on total parenteral nutrition (TPN), then 3 times
carbonate, BUN, creatinine, per week while on long-term TPN
calcium, magnesium
Phosphorus Three times per week until stable on TPN, then weekly
Ionized calcium With consistent low serum calcium
Liver function tests, albumin, Three times per week until Day +30, then weekly while on TPN
total bilirubin
Prothrombin time Weekly while on multiple antibiotics
Vitamin D (25 OH D2+D3) Pre-transplant; then every 3 months until one year
Zinc1 When increased losses are suspected
Manganese, copper, selenium Monthly when on long-term TPN (4-6 weeks)
Triglycerides Weekly while on intravenous lipid emulsion
Weights Daily while an inpatient, then with every outpatient visit
Input/Output Daily while an inpatient
1
Clinical discretion should be used when evaluating zinc levels, keeping in mind that zinc levels in
blood do not reflect tissue stores
G. Follow-up Guidelines after

Completion of Therapy
Survivors of cancer in childhood are at risk for many long-term adverse effects of
therapy. Lifestyle changes, including dietary modification, may help with the management of
some of those sequelae. Dietary recommendation at discharge are listed in Table 14. Survival
rates are increasing for most children with cancer. The 5-year survival rates for all cancers
combined in high income countries has improved from 58.1% in 1975–77 to 83% for ages 0-
4 years; 81.2% for ages 5-9 years; 82.7% for ages 10-14 years; and 82.8% for ages 15-19
years in 2001-2007 [133]. The progress in survival rates is attributable largely to
improvements in treatment and advances in research.
Table 14. Discharge planning for pediatric oncology

patients may include any or all of the following
 Education on high-energy/high-protein diet

 Education on the following diets: low bacteria or food safety, and lactose free
 Graft-versus-host disease (GVHD) bland
 Mucositis
 Provision of oral supplement of choice and instruction on how to use
 Provision of appetite stimulant and education on daily dosage
 Education on how to keep dietary records
 Education on parenteral nutrition (PN) or enteral nutrition (EN)
Follow-up with outpatient dietitian as needed

The Children’s Oncology Group has developed Long-Term Follow-up Guidelines for
Survivors of Childhood Adolescent and Young Adult Cancers [134]. These guidelines
represent a statement of consensus from a panel of experts in the late effects of cancer
treatment in young people. The current version of the COG-LTFU Guidelines (Version 3.0) is
available online (www.childrensoncologygroup.org).
Diet and Physical Activity for Survivors
The American Institute for Cancer Research (AICR) also has guidelines for cancer
survivors: Nutrition and the Cancer Survivor [135]. The three key areas to reduce cancer risk
are weight, diet, and physical activity. The most recent recommendations from the World
Cancer Research Fund (WCRF) / AICR second expert report (WCRF/AICR, 2007) are
applicable for prevention of a secondary tumor or a recurrence. Table 15. lists the ten
recommendations for cancer prevention.
Table 15. Recommendations for cancer prevention
1. Be as lean as possible without becoming underweight.

2. Be physically active for at least 30 minutes every day.
3. Avoid sugary drinks. Limit consumption of energy-dense foods.
4. Eat more of a variety of vegetables, fruits, whole grains and legumes
such as beans.
5. Limit consumption of red meats (such as beef, pork and lamb) and
avoid processed meats.
6. If consumed at all, limit alcoholic drinks to 2 for men and 1 for women
a day.
7. Limit consumption of salty foods and foods processed with salt
(sodium).
8. Don't use supplements to protect against cancer.
9. *It is best for mothers to breastfeed exclusively for up to 6 months and
then add other liquids and foods.
10. *After treatment, cancer survivors should follow the recommendations
for cancer prevention.
And always remember – do not smoke or chew tobacco

*Special Population Recommendations. Anyone who has received a diagnosis of cancer should receive
specialized nutritional advice from an appropriately trained professional.
Additional recommendations covered in the Nutrition and the Cancer Survivor guidelines include:
1. Rethink the ratio of plant foods to animal foods (aim for two thirds or more plant-
based foods)
2. Cook with care (marinate meats; don’t cook meats directly over the flame; avoid
charred or burnt meat)
3. Handle food safely (keep hands, counters, dishes, cutting boards and utensils clean;
wash fruits and vegetables thoroughly; use separate dishes/chopping boards/utensils
for preparing raw meat, fish or poultry; thaw frozen food in microwave or
refrigerator).
H. Prevention
Causes of cancer in childhood are largely unknown. Small numbers are associated with
Down syndrome, other chromosomal and genetic abnormalities, and ionizing radiation
exposure. Nutrition plays an important role in many aspects of cancer development, treatment
and long term survival. Recently, maternal diet and breastfeeding have been studied in
relation to the development of cancer during childhood [136][137][138]. Some studies
suggest that breastfeeding and a maternal diet containing folate and antioxidants during
pregnancy can prevent some cancers in children [139][140].
I. Gaps in Knowledge and Opportunities

for Research
There are numerous gaps in our knowledge concerning the interaction of nutrition with
cancer in children and adolescents. These include the effects of nutritional interventions on
cancer outcomes and the influence of such interventions on co-morbidities; all providing rich
Conclusion
Cancer is the leading cause of disease-related death in children and adolescents in the U.S
and Canada. In the U.S. every year more than 12,000 children are diagnosed with cancer;
approximately 155 new cases per million in the age group less than 15 years. Cancer is highly
curable in young people. In high income countries the survival rate is 80% or higher.
However, more than 80% of children live in low and middle income countries where the
survival rate may be as low as 5%.
Nutrition plays an important role in many aspects of cancer development, treatment and
long term survival. The nutritional status of children when diagnosed with cancer can affect
the outcome of treatment. Malnutrition, in the form of under and overnutrition, has a negative
impact on the survival rate. Malnourished children are at an increased risk for treatment-
related complications, reduced tolerance to therapy, altered drug metabolism, increased
susceptibility to infection, and poorer treatment outcome. Anti-cancer treatment itself affects
the nutritional status of patients and contributes to malnutrition. The severity and variety of
side effects will depend on the nature of the disease and the treatment protocol used. Common
side effects interfering with nutrition are nausea, vomiting, loss of appetite, alteration of taste,
mucositis, pneumatosis intestinalis, and colitis. In those who have undergone hemopoietic
stem cell transplantation, graft versus host disease (GVHD) may result in an additional
nutritional challenge. On the other hand, prolonged steroid use, physical inactivity and certain
changes in metabolism predispose children to obesity. Malnutrition precludes optimal healing
and recovery from therapy; therefore maximal effort should be focused on its prevention and
treatment. Nutritional assessment of children diagnosed with cancer is important for targeting
dietary intervention. Special attention should be paid to metabolic derangements of
macronutrients, leading to protein energy malnutrition, and micronutrients such as

deficiencies of vitamin D, vitamin K, zinc, copper and selenium. Dietary intervention
includes the use of dietary supplements, modular boosters, appetite stimulants, probiotics,
enteral and parenteral nutrition. Specific diets may be used during treatment, such as in
periods of neutropenia, GVHD and other circumstances. Survivors of cancer in childhood are
at risk for many long term adverse effects of therapy. Lifestyle changes, including dietary
modification, may help with the management of some of those sequelae. But there are
numerous gaps in our knowledge concerning the interaction of nutrition with cancer in
children and adolescents. These include the effects of nutritional interventions on cancer
outcomes and the influence of such interventions on co-morbidities; all providing rich
Patient Education Resources

Recommendations for Patients to Manage Treatment-Related Side Effects
Alterations in Taste and Smell

 Decreased taste sensation
o Select appealing foods; consider smell, texture and appearance. Bright colors
attract interest.
o Red meat may taste different; substitute poultry, fish, eggs, or other protein-rich
foods.
o Avoid foods that do not look and/or smell good.
Try cold foods: cold sandwiches, cheese, shakes.
o Try foods at room temperature.
 Dental problems
o Rule out dental problems as the source of strange tastes.
o Ask your dentist about good mouth care.
Mouth and Throat Problems

 Sore mouth or throat, difficulty swallowing, and jaw pain
Try soft and/or pureed foods that are easy to chew and swallow.
o Cook foods until they are tender.
o Cut foods into small pieces.
o Use a blender to puree food and add gravies or sauces to moisten.
o Use a straw to drink liquids.
o Try foods at room temperature.
o Adjust swallowing technique by tilting head back or moving it forward.
o Rinse your mouth with water after eating to remove residual food and bacteria.
o Ask your doctor about anesthetic lozenges and sprays for the mouth and throat.
o Ask yourdentist/doctor to recommend a product to coat/protect mouth and throat.
o Avoid foods that are irritating, such as rough, coarse foods; spicy or salty foods;
and acidic foods like chili pepper. Replace citric fruits and juices with nectars.
 Dental problems
o Maintain regular dentist visits.

o Use a soft toothbrush and/or toothpaste for sensitive teeth/gums.
o Avoid candies or gum that contain sugar; try sugar-free gum or candy instead.
o Avoid sticky foods like caramel or chewy candy bars.
o Ask your dentist/doctor to recommend a product to coat/protect your mouth and
throat.
o Ask your dentist to recommend a special cleaning product if gums and mouth are
sore.
 Dry mouth
o Use a blender to puree food and add gravies to moisten.
o Use lip salves to keep lips moist.
o Sip on water or ice chips every few minutes.
o Sweet/tart foods produce more saliva—this is not indicated with sore mouth or
throat.
o Suck on sugar-free hard candy, popsicles, or sugar-free gum—produces more
saliva (if mouth and throat are not sore).
o Ask your dentist/doctor to suggest artificial saliva.
Gastrointestinal Complications
 Cramps, bloating and gas, heartburn, getting full quickly and easily
o For heartburn, sit up or stand for about an hour after eating.
o Rest after meals (sitting up); do not participate in vigorous activity.
o Wear loose-fitting clothing.
o Avoid eating 1 to 2 hours before cancer treatment.
o Avoid gas-producing foods such as broccoli, cabbage, cauliflower, beans, lentils,
and onions.
o Eat small amounts often and slowly.
o Ask your doctor about medications.
 Diarrhea
o Drink plenty of liquids to prevent dehydration.
o Consume small amounts of food throughout the day vs. three large meals.
o Replenish sodium and potassium.
o Eat a low-fiber diet.
o Avoid grease, fat, raw foods, spices.
o Drink liquids at room temperature.
o Limit caffeine, strong teas, soda, and chocolate.
o Rule out lactose intolerance.
 Constipation
o Drink plenty of liquids.
o Drink something hot 30 minutes before expected bowel movement.
o Eat a high-fiber diet.
o Ask your doctor about stool softener/laxative.
Anorexia/Cachexia
 Nausea and vomiting
o Keep track of when nausea and/or vomiting occurs and the potential cause in a
food diary.
o Avoid hot foods—these add to nausea.
o Avoid favorite foods during periods of nausea and vomiting.
o Avoid greasy, fried, or heavily spiced foods.
o Eat crackers or Melba toast before getting out of bed.
o Ask your doctor about antiemetics.
o Eat small amounts often and slowly.
o Avoid eating in rooms with strong odors.
o Drink fewer liquids with meals—these can cause a bloated feeling.
o Drink/sip liquids throughout the day.
o Drink cool/cold beverages.
o With vomiting, avoid trying to drink or eat until it is resolved.
o Drink small amounts of clear liquids until vomiting is controlled; then advance
to full liquids and eventually a soft and/or regular diet.
 Loss of appetite
o Ask your doctor about an appetite stimulant.
o Keep snacks handy and munch throughout the day.
o Ask your dietitian/doctor about adding nutrients to diet with supplements.
o Serve small food portions on small plate.
o Stay calm at mealtimes; don’t rush to finish meals.
o Question depression; consult a psychiatrist.
o Encourage eating with others, such as family or friends.
o Eat whenever hungry; don’t restrict intake to mealtimes only.
o Take advantage of good days to increase your food intake.
Weight Gain
 Delay dieting/losing weight until the cause of weight gain is identified.
 Follow no concentrated sweets/no added salt diet if weight gain is attributed to
steroids.
 Use glycemic load method to plan meals if insulin resistance is suspected.
 Use a hunger scale.
 Exercise regularly unless it is contraindicated.
 Try to identify emotional and environmental reasons for overeating and snacking.
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Chapter II
Calcium Supplementation
in Young Children in Asia:
Prevalence, Benefits and Risks
Shu Che, Colin Binns and Bruce Maycock

School of Public Health and Curtin Health Innovation Research Institute,
Curtin University, Perth, Western Australia
Abstract
Calcium is essential for maintaining bone health in infants and young children. The
calcium intakes of weaning infants and children in Asia are relatively low in comparison
to their Western counterparts. This is an increasing concern for Asian parents and is one
reason the Asia Pacific region is becoming a large market for vitamins and dietary
supplements. However, there is a lack of data on the long-term benefits to early calcium
supplementation of healthy infants and young children.
The objective of this chapter is to discuss the appropriate calcium intakes for infants
and young children, the risks and benefits of calcium supplementation and to review the
proportion of children in Asia who are taking calcium supplements. To achieve our
objective a literature review was undertaken of the English language databases PubMed
and Web of Knowledge. Studies were selected that reported outcomes of calcium intake
in infants and young children, as well as systematic reviews of such studies.
Studies were undertaken of children in China and a comparison group of Chinese
children living in Australia to document the use of calcium supplements. The prevalence
of dietary supplementation among children under five years old in China (30.0%) was
higher than in Australia (21.6%). In supplement users in China, 60.3% of them took
calcium supplementation while only a small number in Australia (8%) took calcium
supplements. Age and feeding method of the child (ever breastfed or not) were associated
with nutritional supplementation in Australia, while household income and mother’s
educational status were significantly related to the use of dietary supplements including
calcium supplements in China. More than half of the children took supplemental calcium
44 Shu Che, Colin Binns and Bruce Maycock
in the form of calcium gluconate (51.8%) and the average intake from supplements was
131 mg per day.
There is little evidence to support the general use of calcium supplements in infants
who were exclusively breastfed or formula fed. Evidence from recent studies does not
support the use of calcium supplementation in healthy children as a public health
intervention. However, for weaning infants and children with low calcium intakes,
increased intake of calcium-rich foods should be encouraged. If adequate calcium cannot
be achieved through food sources, supplementation may be an effective alternative. More
studies are required in infants and young children with low calcium intakes, particularly
those living in Asian countries or children of Asian ethnic origin.
Abbreviations
EAR Estimated Average Requirement
RDA Recommended Dietary Allowance
AI Adequate Intake
UL Tolerable Upper Intake Level
PRI Population Reference Intakes
RI Recommended Intakes
BMC Bone Mineral Content
BMD Bone Mineral Density
DRI Dietary Reference Values
RDI Recommended Dietary Intakes
NRV Nutrient Reference Values
CV Coefficient of Variation
SD Standard Deviation
WHO World Health Organization
NHMRC The Australia National Health and Medical Research Council
FAO The Food and Agriculture Organization of the United Nations
IOM Institute of Medicine
SCF Scientific Committee on Food
US United States
Introduction
Adequate calcium intake is important for bone health throughout the lifespan [1]. It is
required for the normal development and maintenance of the skeleton as well as for the
proper functioning of neuromuscular and cardiac function [2]. Providing adequate dietary
intakes of calcium during infancy and early childhood may not only prevent diseases
influence immediate health but may also delay or prevent osteoporosis in the elderly [3-7].
Although calcium is essential for maintaining bone health in infants and young children,
the calcium intakes of weaning infants and children in Asia are relatively low in comparison
to their Western counterparts. This can be partly attributable to the high incidence of lactase
deficiency in Asia children, non-milk based diets, poor dietary habits in some families,
Calcium Supplementation in Young Children in Asia 45
inadequate information and knowledge on calcium rich foods of parents [1, 8, 9]. The
prevalence of primary lactase deficiency is almost 100% in Asian adults and approximately
20% of Asian children younger than 5 years of age have evidence of lactase deficiency and
lactose malabsorption [10-13]. Dietary lactose enhances calcium absorption and, conversely,
lactose-free diets generally have lower overall calcium content and also lower calcium
absorption [14]. Thus, lactose intolerance (and lactose-free diets) theoretically may
predispose to inadequate bone mineralization [15, 16]. It is reported that about 20% of 1-2
years old and 45% of 3-5 years old children fail to achieve the recommended intake of
calcium in the USA [17]. Considering the high prevalence of lactose intolerance and low
consumption of calcium-rich food in Asia, it may be even more difficult to achieve
recommended intakes without calcium supplementation for Asian children. The pattern of
complementary feeding in many Chinese infants and young children, especially in rural areas,
does not conform to current WHO recommendations for complementary feeding, including in
achieving calcium intakes [18].
Dietary supplements enriched with vitamins, minerals, and other substances have
received increasing attention worldwide. The North America and the Asia Pacific regions are
the dominant markets for vitamins and dietary supplements [19]. A cross-sectional study of
infants aged 6-12 months (n=251) in Beijing found that calcium supplements and cod liver oil
were prescribed by health care providers for prevention of rickets in 71.6% and 49% of
infants, respectively [20]. However, evidence for the association between calcium
supplementation and bone changes are insufficient at present to make general
recommendations for widespread use. There is also a lack of data proving long-term benefits
to early calcium supplementation of healthy infants and young children [6]. A recent meta-
analysis showed that although there is a small benefit of giving calcium supplements to
children, it is unlikely to substantially reduce fracture risk in later life or even result in a
clinically significant decrease in fracture risk in children [21]. In this chapter, we consider
normal and abnormal patterns of bone mineralization in infants and sources of calcium in
infants and pre-school children aged from 0 to 60 months. We further consider long-term
effects of potential interventions related to calcium. To achieve our objective a literature
review was undertaken of the English language databases PubMed and Web of Knowledge.
Studies were selected that reported outcomes of calcium intake in infants and young children,
as well as systematic reviews of such studies. All abstracts were read and relevant full text
publications were then retrieved to include in this review.
Review of Calcium Recommendations in Infants

and Young Children
Calcium requirements vary in different ethnic groups for dietary, genetic, body size,
physical activity, lifestyle, and geographical reasons [22, 23]. Different bone mass and its
accretion rate are evident among Asian, African, Caucasian and Hispanic adolescents [24-26].
Ethnic differences in fractional calcium absorption were also found in studies. Comparing to
Caucasian counterparts, Chinese children and adolescents have higher fractional calcium
absorption [27-30].
A recent study compared calcium and bone accretion between Chinese adolescents and
American Caucasian populations. Although habitual calcium intakes and vitamin D status
were found to be lower in Chinese adolescents, bone mineralisation from age 10-15 years was
similar in the two groups [31]. It further suggested more efficient calcium utilization, calcium
absorption, excretion, and retention among the Chinese and calcium absorption efficiency
decreased with increasing calcium intakes for the Chinese girls, but not the Caucasian girls.
This suggested that bone accretion could be matched between the different ethnic groups at
higher calcium intakes [31].
However after considering the ethnic differences in calcium metabolism and bone
accretion in skeletal development, different calcium allowance recommendations were
developed for different populations. Definitions for the terms used including Dietary
Reference Values (DRIs)/ Recommended Dietary Intakes (RDIs)/Nutrient Reference Values
(NRVs) for calcium requirements are given below [32-34]:
Box 1. Definitions given to DRIs/RDIs/NRVs
Estimated Average Requirement (EAR) – Reflects the estimated median

requirement and is particularly appropriate for applications related to planning and
assessing intakes for groups of persons.
Recommended Dietary Allowance (RDA) – Derived from the EAR and meets or
exceeds the requirement for 97.5 percent of the population.
Adequate Intake (AI) – Used when an EAR/RDA cannot be developed; average
intake level based on observed or experimental intakes.
Tolerable Upper Intake Level (UL) – As intake increases above the UL, the
potential risk of adverse effects may increase. The UL is the highest average daily
intake that is likely to pose no risk of adverse effects to almost all individuals in the
general population.
Recommended Nutrient Intake (RNI) – It is the daily intake, which meets the
nutrient requirements of almost all (97.5 percent) apparently healthy individuals in an
age and sex-specific population group.
Population Reference Intakes (PRI) – the level of (nutrient) intake that is adequate
for virtually all people in a population group.
Calcium as a nutrient is most commonly associated with the formation and metabolism of
bone [32]. At full-term birth, the human infant has accrued about 26 to 30g of calcium, most
of which is in the skeleton [32]. When calcium transfer from the placenta ceases at birth, the
newborn infant is dependent on dietary calcium [32]. Human milk is recognized as the
optimal source of nourishment for infants and the optimum source of calcium [35, 36]. The
2011 Institute of Medicine committee stated that there were no reports of any full-term,
vitamin D–replete infants developing calcium deficiency when exclusively fed human milk
[32]. The breastfed full-term infant is assumed to have a sufficient calcium intake regardless
of the actual intake [6]. Therefore, AIs for calcium for infants up to 6 months old are based on
average intake of breastmilk during the first half year of life and the studies that have
determined average concentration of calcium in breastmilk [32, 37]. Reasonable estimations
of calcium absorption, accretion and excretion are also taken into account [32]. In formula-
fed infants, it is assumed that calcium is less bioavailable from infant formula compared to
breastmilk [6]. Statutory guidance in the United States, and common practice throughout the
world, is to provide 30% to 100% more calcium in infant formula than in breastmilk [6].
Therefore, the AIs for infants 7–12 months were set by not only considering the calcium
intake from breastmilk or infant formula at this age but also an estimate of intake from
supplementary foods [2]. The EARs for young children under 5 years old were set by
estimating calcium requirements from data on daily rates of calcium accretion from a typical
diet and then evaluating, on the basis of available balance data of the target population, the
amount of calcium needed in the diet to achieve the requirements [6]. The RDAs were set by
additional considering the variability of this intake to achieve the accretion in nearly all
children [6]. The UL for calcium is not a recommended intake. Rather, it is intended to
specify the level above which the risk for harm begins to increase. It is defined as the highest
average daily intake of a nutrient that is likely to pose no risk of adverse health effects for
nearly all persons in the general population [32]. As intake increases above the UL, the
potential risk for adverse effects increases. Only a limited number of studies have reported the
toxicity doses of calcium of children 1 to 5 years. Values for the UL were not set for infants
or young children for all the populations. In the USA the ULs were set on the basis of limited
available safety data and suggested that calcium toxicity was extremely unlikely to occur in
healthy infants unless high-dose supplementation would be provided [32].
Australia and New Zealand
The Australia National Health and Medical Research Council (NHMRC) and the New
Zealand Ministry of Health developed the Australian/New Zealand RDIs in 2006, which were
based on an update of the 2001 USA values. The AI of calcium for Australian and New
Zealand for 0–6 months was set based on the estimated average intake of breastmilk (780
ml/day) and the average concentration of calcium in breastmilk (264 mg/L). After considering
the lower bioavailability of calcium in infant formula, 350 mg/day was recommended for
formula-fed babies (Table 1).
In the 2006 Australian/New Zealand RDIs, the a mean intake of breastmilk was considered to
be 600 ml/day at 7–12 months with an average concentration of 210 mg/L [2]. Based on this
data an intake of 140 mg/day calcium from complementary foods is required during the
second six months of life. This resulted in a calculated calcium intake of 266 mg/day, which
was rounded up to 270 mg/day [2] (Table 1).
For children 1–8 years, the daily net absorbed calcium need was estimated to be 220
mg/day. By assuming absorption rates of one standard deviation (SD) above those of adults
and considering an approximate body weight for this age group, a figure of 360 mg/day was
given as the EARs for 1–3 year-olds and 520 mg/day to the older group to provide this level
of absorbed calcium [2]. The RDI was set assuming a coefficient of variation (CV) of 15%
for the EAR and after rounding, giving an RDI of 500 mg/day for 1–3 year-olds and 700
mg/day for 4–8 year-olds [2] (Table 1).
As there is little evidence of toxicity in children, the UL was set at 2,500 mg/day by
considering the calcium dosage when adverse effects are found in adults with renal stones and
considering the need to prevent interference with zinc and iron absorption [2] (Table 1).
Table 1. Current Dietary Reference Intake values for calcium for infants and young children (mg/day)
Australia and New WHO 2002 United States and Canada 2011 European Japan 2010 China 2010
Zealand 2006 Union
1993
AI UL RNI AI EAR RDA UL PRI AI EAR RDA AI UL
Males Females Males Females
0–6 months Breastmilk Breastmilk 200 1000 200 300

210 300
Formula 350 Formula 400
6–12 months 270 400 260 1500 400 250 400
1-2 years 360 2500 500 500 700 2500 400 350 350 400 400 600 2000
3 years 360 2500 500 500 700 2500 400 500 450 600 550 600 2000
4-5 years 520 2500 600 800 1000 2500 450 500 450 600 550 800 2000
AI, adequate intake; UL, tolerable upper intake level; RNI, recommended nutrient intake; EAR, estimated average requirement;
RDA, recommended dietary allowance; and PRI,Population Reference Intakes.
World Health Organization
The Food and Agriculture Organization (FAO) of the United Nations and the World
Health Organization (WHO) expert consultation had produced a publication on defining
standards for micronutrient requirements in 1998 [34]. The recommendations for calcium
allowances were based on Western European, American and Canadian data [34]. For infants,
the concentration of calcium in breastmilk formed the basis of recommendations of calcium
intakes in infants [22].
The FAO/WHO determined the daily calcium increment in the skeleton is about 100 mg
in the first two years of life using data from American Academy of Pediatrics Committee on
Nutrition [22, 38]. Together with information on the urinary calcium of infants and insensible
losses of 20 mg/day, infants calcium absorption need was calculated as 120 mg daily to allow
for normal growth [22]. For breastfed babies, a mean intake of 240 mg was assumed to meet
the need of 120 mg net absorption. Based on the average daily breastmilk production of 750
ml, the calcium recommended intake of 300 mg for breastfed babies can be achieved. With
cow milk, calcium intake needs to be set at about 300 mg to meet the requirement of 120 mg
net calcium absorption and 400 mg of calcium intake was the recommended (Table 1).
From age 2 to 9 years, as whole-body calcium increases with skeletal growth, the daily
rate of calcium accumulation rises to 120 mg and urinary calcium increases to 60 mg. A
dermal loss of 40 mg is added to these figures leading to an average daily net absorbed
calcium requirement of 220 mg during this period [22]. Assuming that the net absorption of
calcium by children is one SD above that of adults, the average daily requirement during this
period is about 440 mg and the average recommended intake is 600 mg [22] (Table 1).
United States and Canada
The National Academy of Sciences, Institute of Medicine (IOM) released their new DRIs
for calcium and vitamin D intake for the United States and Canada in 2011 [32]. Using
estimates of a mean calcium concentration in breastmilk (259 mg/ml) and the amount of milk
consumed per day (780 ml), the AI for calcium for infants 0 to 6 months of age is 200 mg/day
(Table 1). It is a value reflective of the calcium provided to exclusively breastfed infants and
to be considered as sufficient amounts of calcium to meet most infant’s growth needs by 2011
IOM committee [32].
From 6 to 12 months of age, the intake of calcium from solid foods becomes more
significant. The IOM 2011 committee determined that the mean calcium intake from solid
foods was about 140 mg/day for formula fed infants based on the limited data and assumed
that breastfed babies had similar intakes of solid food to those of formula fed infants of the
same age. Based on the mean breastmilk intake during the second 6 months of life (600
ml/day) and a calcium concentration (200 mg/L) in breastmilk during this age span, the
calcium intake from breastmilk would be approximately 120 mg/day. Adding those figures
together gives a total intake of 260 mg/day [32] (Table 1).
From the results of studies that used children as subjects, the 2011 IOM committee used
the average bone calcium accretion to set an EAR rather than an AI for young children older
than one year [32]. An estimated EAR is established as 500 mg of calcium per day, rounded
from 474 mg/day by the 2011 DRI panel for children 1 through 3 years of age. An additional
30% calcium retention would meet the needs of 97.5% of age group 4 to 8 years. This results
in an estimated RDA for calcium of 700 mg/day calcium, with rounding [32] (Table 1).
Studies of Abrams et al. and Ames et al., indicate a calcium intake of 800 mg/day could
be expected to achieve the levels of calcium needed for bone accretion for Children 4 through
8 years of age [39, 40]. Again, the assumption that another approximately 30% is needed to
cover about 97.5% of the population results in a calculated and rounded RDA value for
calcium of 1,000 mg/day [32] (Table 1).
Within the confines of the limitations of the data, a ‘no observed adverse effect’ level of
1750 mg/day was established for infants [32]. To reduce the uncertainty factor, the UL for the
life stage group of 0 to 6 months was adjusted for weight difference and rounded to 1,000
mg/day [32]. Given the limitation of data, a slight uncertainty correction is warranted, and the
UL is set at 1,500 mg/day for infants 7 to 12 months of age [32] (Table 1).
A UL of 2,500 mg of calcium per day was continually used for children between the age
of 1 and 8 years as it was established in 1997 [41] (Table 1). New data on adverse outcomes
due to over-dose of calcium intake among children have not emerged since then. Given the
expected body weight and metabolic capacities increases for old ages, the level of 2500
mg/day is a reasonable compared with the new UL set for infants [32].
European Union
The population reference intakes defined by the Scientific Committee on Food (SCF) in
1993 are based on a factorial approach without considering measurements of bone mineral
accretion under different calcium intakes [33]. The 1993 SCF estimated the mean calcium
retention needed per day for skeletal growth was 150 mg/day. The PRI is 400 mg/day for
infants in the second half of the first year and for children up to age 3 years, 450 mg/day for
children between 4 and 6 years [33]. Those figures were based on the assumption that the net
absorption of dietary calcium is 35% and 30% were added to the calculated amount to allow
for individual variation [33]. Because of the absence of reliable data, the PRI for 6-11 months
old infants was taken as the same as for 1-3 years olds [33].
Possible adverse health effects of individual micronutrients at intakes in excess of dietary
requirements have been evaluated in European population groups. It was reported that
European infants and young had a high intake of calcium [42]. Although there are no data to
set a numerical UL for children and adolescents and no appreciable risk has been identified
even with the extreme levels of calcium intake in this age group [42].
China
At present insufficient evidence is available from Chinese studies to establish EARs for
calcium intake from which RDAs would be determined. Therefore, the AIs were established,
based on maximal calcium retention for different age groups. The AI for calcium is 300
mg/day for infants before 6 months and 400 mg/day for infants 6 to 11 months. A calcium
intake of 600 mg/day is recommended to children aged 1 to 3 years. An AI of 800 mg/day
was given for 4-10 year-olds [43] (Table 1).
The UL for calcium was set at 2000mg/day for Children aged 1-6 years old by the
Chinese Nutrition Society [43] (Table 1).
Japan
The AI for calcium is 200 mg/day for infants of 0-5 months and 250 for infants of 6-11
months. The EAR and RDA for calcium for 1-2 years old children is 350 mg/day and 400
mg/day respectively. The EAR and RDA of calcium for boys in 3-5 years are 50 mg higher
than that for girls in the same age group [44] (Table 1).
Calcium Intakes of Children in Asia
Calcium intakes vary between countries, generally following the different dietary habits
and depending largely on dairy product consumption [22]. The FAO/WHO reported the daily
protein and calcium intakes in different regions of the world during 1987 and 1989, the lowest
calcium intakes occur in Asia, and the highest in North America and Europe [22]. Some study
results further indicate variation in calcium intake among child and adolescent ethnic groups.
Asians as the ethnic group were found with relatively low calcium intakes in comparison to
the Western counterparts [45-48].
Milk or milk products are a good source of many nutrients and the best known food
source for calcium. Dairy products provide calcium in a readily absorbable and convenient
form. Human milk is the best source of calcium for infants, averagely providing the infant
with 202 mg of calcium per day in the first half year and 120 mg per day in the second half
[32]. The calcium concentration in milk is 120 mg per 100 g and up to 1100 mg/100 g milk
products, from which about 32% is absorbable [49]. The average calcium contribution from
milk differed among ethnic groups. Lactose restriction reduces milk consumption in Asians
who have the highest prevalence of lactase deficiency in the world, close to 100% [12, 13].
The incidence of of some degree of lactase deficiency in Shanghai children aged 0～6 years
was reported to be 47.4% and lactase intolerance was 16.5%, with a trend of increasing with
the age [50].
Only a small number of studies have examined sources of calcium from foods and
beverages as consumed by Asian populations especially in the child age group. A study in the
US on ethnic diversity and calcium intakes found that vegetables and legumes were a major
source of non-dairy calcium for Asian Americans, who generally had lower dairy
consumption when compared to other population groups. The Asian Americans were reported
to consume only 10% to 11% calcium from dairy products [46]. Similar results were found in
China, where the main sources of calcium were vegetables (35.2%), bean and bean products
(13.9%), wheat (11.2%) and rice (9.1%) and less than 5% of calcium came from dairy foods
[51]. Those figures were extracted from 2002 China National Nutrition and Health Survey
where it was reported that the deficiency of calcium was a common problem in Chinese
residents [51]. In children aged 2 and 3 years, only 3.7% males and 5.1% females met the AI
for calcium intake (600 mg/day), which were the highest in all age groups of each gender. In
4-6 years age group, the percentage of meeting the AI (800 mg/day) dropped to 1.8% for
males and 1.1% for females [51].
Prevalence of Use of Calcium Supplements

in Australia and China
Although calcium intake can be increased by dietary means, long-term adherence to high-
calcium diets is difficult to achieve for Asians, as they often report having a low dairy
consumption [18, 46, 51, 52]. Calcium supplements may be a useful way of helping Asians to
obtain sufficient calcium and enhance health and wellbeing [53].
Most studies on calcium supplements have focused on adults or older persons and little is
known regarding the intake of calcium supplements by infants and young children. A recent
study from Taiwan reported that 34.9% of the infants had been given a dietary supplement
and 15.5% took calcium supplement between birth and 6 months of age [54]. A survey of
infant feeding practices (n=251) in Beijing, China found that 71.6% infants aged 6-12 months
were taking calcium supplementation [20]. In Hubei, PR. China, a survey reported a
prevalence of 90.2% (1523/1688) of calcium supplementation in pre-school children in four
kindergartens and more than half of them were taking calcium supplements without medical
prescriptions [55]. Australians have a high prevalence of taking dietary supplements. A
representative population survey conducted in 2004 in South Australia reported the use of
vitamin supplements by 39.2% respondents and mineral supplementations by13.6% of the
population [56]. No recent data is available on the use of calcium supplements by infants or
young children in Australia.
Until recently, few studies have investigated the intake of calcium dietary supplement by
infants and young children under five years old. And there have been no studies of calcium
supplementation among Chinese children under five years in mainland China or overseas
published in English. To document the prevalence of use of calcium supplements in these
populations, a survey was carried out of Chinese mothers living in Perth, Australia and
Chengdu and Wuhan, PR China.
The China Australia Supplements Study

(CASS Study)
A survey was undertaken of 231 Chinese mothers living in Perth Australia, 360 mothers
living in Wuhan and 1335 in Chengdu, PR China. The participants in Perth were mothers
with children under 5 years old who were recruited from the Perth Chinese community,
including Chinese schools and community organizations. A total of 238 mothers agreed to
participate with a response rate of 96.0% and 231 mothers completed the dietary
supplementation questionnaire, a final response rate of 93.1%. Participants in China were
recruited from kindergartens in Wuhan and Chengdu. A total of 2800 questionnaires were
distributed by kindergarten teachers and 1702 and 556 were returned by the mothers in
Chengdu and Wuhan respectively. The dietary supplementation questionnaire was completed
by 1335 mothers in Chengdu and 360 mothers in Wuhan, a total response rate of 60.5% in
China. The study was approved by the Curtin University Human Research Ethics Committee.
Demographic and breastfeeding information was collected using a validated and reliable
questionnaire previously used in Chinese population studies [57]. Mothers were classified
into three groups to compare their economic status based on the local annual household
income [58, 59]. Data were analysed using the IBM Statistical Package for Social Sciences
(SPSS) Version 20.0. Independent samples t-test was used to compare means between groups.
Chi-square (χ2) test was used to test associations between basic characteristics and factors
potentially related to the use of supplements among young children. P values <0.05 were
considered statistically significant.
Results of the CASS Study

A total of 231 Chinese mothers living in Perth Australia and 1355 mothers living in
Chengdu, Sichuan Province and 360 mothers living in Wuhan, Hubei Province, PR China
completed the supplement questionnaire. The distribution analysis shows no difference in
age, education attainment, marital status, working status, family income status, breastfeeding
initiation and duration, between mothers who completed the supplement questionnaire and
mothers who did not.
There was also no difference in education attainment, marital status, family income
status, breastfeeding initiation and duration, between mothers in Chengdu and Wuhan. The
only two statistically significant differences between mothers in Wuhan and Chengdu were
the average age (31.2 years in Chengdu and 30.8 years in Wuhan, p<0.001) and working
status (68.7%Wuhan mothers have full-time work compared to 60.1% in Chengdu, χ2=8.1,
df=2, p<0.05). Because the differences are so small in Wuhan and Chengdu mothers, their
data have been combined into one group.
A total of 21.6% of the Chinese children living in Perth were taking dietary supplements,
including multivitamins/minerals, fish oil, probiotics, calcium and vitamin D.
In Chengdu and Wuhan, China, 30.0% of young children were having dietary
supplements and 60.3% of those supplement users were taking calcium supplements.
Compared to Chinese Australians, Chinese parents living in China were more likely to give
their children dietary supplements (χ2=6.9, df=1, p<0.001) and especially calcium
supplements (χ2=40.3, df=1, p<0.001). About half of the Chinese children taking calcium
supplements were also taking Vitamin D (including the use of multi-vitamins) (Table 2).
Table 2. Prevalence of supplements use by type in Chinese children under 5 years living
in Australia and China
Australia China
% Supplement % Supplement
n % (n=231) n % (n=1695)
Supplement type users users
Any supplement 50 21.6 100 509 30.0 100
Calcium 4 1.7 8 307 18.1 60.3
Calcium + Vitamin D 2 0.9 4 160 9.7 31.4
In Australia, only four children were given specific calcium supplements. One was taking
calcium carbonate tablets, the other calcium lactate, and two were unknown. The most
common forms of supplemental calcium used in Chinese children up to five years old are
gluconate (51.8%) and carbonate (37.5%). The dosage range of calcium supplements for
Chinese children is 54 to 725 mg/day. The average intake for carbonate users (307.4 mg/day)
is higher than gluconate calcium users (81 mg/day) (Table 3).
Table 3. Calcium supplement form and dosage used by Chinese children under five
years in China
Supplements % Calcium Average intake Intake range

form Number supplement users (mg/day) (mg/day)
Carbonate 115 37.5 307.4 (n=106) 85-725
Gluconate 159 51.8 81 (n=154) 54-360
Lactate 11 3.6 - -
Others 9 2.9 116.7 (n=3) 100-150
Unknown 13 4.2 - -
Total 307 100 131.4 (n=264) 54-725
Table 4. Calcium supplement use by maternal and child characteristic variables
Australia China
Any supplement Any supplement Calcium
N p (%) n p (%) n p (%)
Age (year) 0.221 0.675 0.776
≥31 39 (24.5) 194 (30.6) 121 (19.1)
<31 11 (16.2) 212 (31.8) 122 (18.3)
Education 0.268 0.035 0.351
≥University 41 (23.6) 190 (33.7) 109 (19.4)
≤High school 9 (15.8) 216 (28.3) 122 (17.4)
Household income 0.477 0.000 0.001
High 15 (26.3) 93 (35.5) 60 (22.9)
Middle 27 (21.8) 242 (34.6) 139 (19.9)
Low 6 (15.8) 37 (17.3) 22 (10.3)
Gender of the child 0.635 0.549 0.374
Male 28 (23.0) 285 (31.9) 173 (19.4)
Female 22 (20.2) 221 (29.3) 133 (17.6)
Child's age (year) 0.016 0.724 0.687
<1 year 0 8 (29.6) 5 (18.5)
1-2 13 (14.8) 8 (34.8) 6 (26.1)
2-3 11 (21.6) 72 (34.4) 46 (22.0)
3-4 10 (26.3) 201 (32.5) 119 (19.2)
4-5 11 (39.3) 160 (29.7) 97 (18.0)
Infant feeding 0.038 0.192 0.083
Ever breastfed 44 (20.2) 436 (30.8) 267 (18.9)
Never breastfed 6 (46.2) 62 (26.4) 33 (14.0)
In Australia, older children (χ2=12.24, df=4, p<0.05) and children who were never be
breastfed (χ2=4.88, df=1, p<0.05) were more likely to take dietary supplements (Table 4). In
China, no specific child characteristics where associated with taking supplements. However
higher household income and higher education of the mother were significantly related to the
use of all types of child supplements as well as calcium supplements (Table 4).
The CASS study assessed the intake of calcium supplements used by Chinese young
children in China and in Australia. It appears to be the first study reporting on the use of
calcium supplements in Chinese young children up to five years old.
In this study, one fifth of Chinese children in Perth were taking at least one nutritional
supplement. Older children and formula fed children were more likely to be given nutritional
supplements, but relatively few were on specific calcium supplements. This may be due to
higher rates of dairy consumption in Australia than in China and less emphasis on calcium
supplements in the lay press. Data from the Australian nationally representative 1995
National Nutrition Survey shows that the mean calcium intakes were 833 mg/day in children
aged 2-3 years and 769 mg/day in children aged 4-7 years, which is higher than the Australian
and New Zealand AI for calcium for those age group and suggest no need for calcium
supplementation [60].
In China 30.0% of young children were taking nutritional supplements and 60.3% of
these supplements users were on calcium supplementation. It was found that nutritional
supplementation including calcium supplementation was more likely to occur among those
children from a higher income family and with higher educated mother. However, the average
intake of calcium from supplementation was only 131.4 mg per day, which is about 20% of
the AI for calcium for Chinese children in this age group. It is less than half of calcium
consumption that can be provided from one serve (250 ml) of milk, besides milk can provide
other nutrients like protein to support child growth [49]. Studies in children regarding calcium
supplementation and bone changes indicate that BMD changes are influenced by baseline
calcium intake, stage of development, and the sites evaluated for BMD [61]. When baseline
habitual calcium consumption is low, larger increments in BMD occur with increased dietary
calcium intake [62]. The average calcium intake from supplements in Chinese young children
(131.4 mg) is lower that all randomized controlled trials studies (nineteen studies) included in
a meta-analysis assessing effects of calcium supplementation on BMD in healthy children.
Calcium supplementation was with a calcium dose of 300-1200 mg per day in those nineteen
studies [63]. Thus, it is not likely that the low calcium intake from supplements would result a
significant change in BMD in children.
Calcium Supplement Form and Absorption
The most common forms of supplemental calcium used in Chinese children are calcium
gluconate and calcium carbonate. More than half of the supplements users choose the oral
solution of calcium gluconate. Elemental calcium is less concentrated in this form, containing
only 9% elemental calcium [64]. Because calcium gluconate contains a lower proportion of
elemental calcium, it is not considered practical for clinical practice. One popular brand of
calcium gluconate contained 54 mg of elemental calcium in a 10 ml bottle. Chinese children
taking calcium gluconate only take an average of 81 mg calcium a day, which is less than
calcium contained in 100 ml milk [49].
Calcium carbonate is the most common and least expensive form of calcium [64].
Generally calcium carbonate provides more elemental calcium with the same number of pills
[65]. It contains 40% calcium and well-absorbed and tolerated in most individuals when taken
with a meal [66]. The bioavailability of calcium carbonate depends on the dosage and
whether they are taken with a meal [44].
It was found to be equivalent to skim milk and orange juice fortified with calcium-citrate
malate [67]. Calcium can compete or interfere with the absorption of iron, zinc, and
magnesium. Therefore, for persons with known deficiencies of these other minerals who
require calcium supplementation, taking calcium supplements between meals is advisable
[64].
Benefits of Calcium Supplantation
Increased Bone Density and Bone Strength

Low bone mineral density is an important risk factor for osteoporotic fractures [68].
Calcium deficiency leads to a reduction in bone mass by increasing bone resorption to
preserve the level of ionised calcium in the extracellular fluid [61].
Dietary calcium deficiency may also be a major cause of rickets in children in developing
countries [61]. Although nutritional rickets has long been considered a disease caused by
vitamin D deficiency, calcium deficiency has also been reported as an important cause of
rickets by recent studies in Nigeria, Bangladesh, India and the US [3, 69-71]. Study did in
Europe also found that low 25-(OH) D level combined with low calcium intakes and possibly
digestive disorders, were associated with an increased risk of genu valgum in children [4].
Optimal calcium intake is especially important during childhood, when most mineral
accretion occurs [72]. Evidence has shown that increased calcium intakes, with and without
vitamin D, increases BMC/BMD in children [73-75]. Studies did in Asia children also
suggest that higher long-term habitual calcium intake and physical activity may lead to higher
BMC in children [76, 77]. A review on calcium supplementations in children reported that
almost all studies (seventeen out of nineteen) resulted a statistically significant improvement
of supplementation on BMD in children [78]. Subjects in eight of the seventeen studies had a
baseline daily calcium intake of 800–1300 mg. Those studies (eight of the seventeen)
concluded that calcium supplementation was efficient even if baseline calcium intake was
adequate [78].
However, evidence for an association between calcium supplementation and bone
changes in children is conflicting [63, 75]. A systematic review evaluated the effect of
calcium supplementation on BMD and concluded that such supplementation has little effect
on BMD in children [63]. The only site with a significant increase in BMD was the upper
limb. This effect translated into a 1.7% greater increase in BMD in the supplemented groups
compared with non-supplemented groups. The review does not support the use of calcium
supplementation in healthy children as a public health intervention [63].
Considering that few Asian children can meet the recommended calcium intakes for their
ages and low BMD is a risk factor for fracture in childhood, increasing their calcium intake
and optimising age appropriate bone mass may have a immediate beneficial effect [79, 80].
Lower Body Fat

Calcium intake has been associated with a reduction of body weight or weight gain in
several studies [81-84]. Although the effect of calcium intake on body composition remains
unclear, it may due to the reduced consumption of sugar-sweetened drinks and increased
resting energy expenditure [82, 84]. A study of a multiethnic sample of children on calcium
intakes and body fat suggested that calcium intake may play a role in fat accumulation and
energy balance through its effects on resting energy expenditure [84].
However clinical, longitudinal, retrospective and cross-sectional studies in children show
inconsistent findings regarding calcium intake and bone changes. Some studies reported no
association between calcium and/or dairy intake in children and weight and/or body
composition [85-87]. A systematic review of placebo-controlled randomized controlled trials
of calcium supplementation found no statistically significant effects of calcium
supplementation on weight, body fat or lean mass [88].
Although the results do not exclude an effect of calcium supplementation with dairy
products on weight gain or body composition, at the present time there is insufficient
evidence to recommend taking dairy products or calcium supplements as a means of
population weight control [88].
Decreased Osteoporosis in Later In Life

Bone loss in later life is related to the quality of peak bone mass established over the first
two decades of life [89]. Considerable studies have been carried out over the past several
decades to discuss whether osteoporosis originates in childhood and if providing high dietary
intakes of calcium may delay or prevent this disease in the elderly [6].
Calcium is the primary bone-forming mineral that must be supplied to the diet and is the
most important during childhood when approximately 200 mg/day is accreted into the
skeleton [90]. Postmenopausal BMD is a function of peak bone mass formed during the first
two decades of life and the rate of subsequent bone loss index during the aging process,
which are equally important risk factors for fracture in later life [91, 92]. One of the
recommended primary preventions of osteoporosis is the adequate calcium intake during
infancy and childhood to optimize the gain in bone mass [5]. Thus, efforts to maximise peak
bone mass through calcium supplementation during childhood have been encouraged.
However, there has been no intervention study long enough to test the effect of
nutritional factors to maximize peak bone mass [1]. It remains unclear that whether increases
of BMD benefited from calcium supplements would persist into later life after
supplementation stopped.
Risks of Excess Consumption of Calcium

There has no report of excess intake of calcium from food sources, however, as the use of
calcium supplements increasing, excess consumption of calcium may occur [93]. Calcium
plays a major role in the metabolism of virtually every cell in the body and interacts with a
large number of other nutrients, like iron, zinc, magnesium and phosphorus，and as a result,
disturbances of calcium metabolism may give rise to a variety of adverse effects [42, 94].
There is no data on children taking calcium from dietary sources or from the usual level
of supplements that provides reliable information on adverse effects. Data from European
populations indicate that the intakes of calcium from all sources in infants can be close to the
UL in a small percentage of the population [42]. In British infants the 97.5th percentile of
calcium intake was 1400 mg/day. In German non-breastfed infants the 90th percentile of
calcium intake was 700 to 900 mg/day [42]. And it was reported by European Commission of
SCF and the Scientific Panel on Dietetic Products, Nutrition and Allergies that no adverse
effects of calcium citrate-malate supplements or extra dairy foods (500 to 1000 mg extra
calcium over 1 to 3 years) were reported in 217 children between 6 and 14 years, in
comparison to un-supplemented controls [42].
Hypercalciuria, as a secondary outcome to high calcium intake, can occur in children.
However, the incidence of kidney stones in children is rare. There is limited evidence
concerning high calcium intakes in young children relative to calcium excretion. In a study
undertaken in 4 to 9 months infants, three infants (6%) who received a calcium-enriched
formula (1700 to 1560 mg calcium per day), developed hypercalciuria [95]. Another study
tested the effects of 1,800 mg/day total calcium (supplementation adjusted on the basis of
dietary calcium questionnaire) in children ages 1 to 6 years reported no diffrence in urinary
calcium/creatinine ratios between children who took 1,800 mg/day calcium and those of
placebo controls [96].
A study by Sargent et al. (1999) provides information relevant to infants and calcium
excretion. Formula with added calcium glycerophosphate (1800 mg of calcium and 1390 mg
of phosphate /L) for 9 months were given to infants aged 3.5-6 months old [97]. Together
with calcium from solid foods, those infants had a mean calcium intake of 1,563 ± 703
mg/day at 9 months. Although the focus of the study was lead absorption, the data
demonstrated that total calcium intakes of about 1,550 to 1,750 mg/day did not affect urinary
calcium excretion. However, these data were insufficient to rule out or conclude that a
definate risk exists for calcium supplements use in infants or young children.
Food Sources of Calcium
Compared to calcium from dietary supplements, calcium from food sources may be
preferable for the evidence of better health outcomes. Two recent meta-analysis from same
group on the effect of calcium supplementation on myocardial infarction and cardiovascular
events suggested that calcium supplements in adults in higher doses with or without vitamin
D have been associated with a modest increased risk of cardiovascular events [98, 99].
However, the effect of an equivalent dose of calcium from dairy products has a lower risk
than calcium supplements and result in lower peaks of serum calcium levels [100].
Additionally，calcium intake from dairy is often reported as a possible factor that may
reduce body weight or weight gain [81-84]. A meta-analysis on twenty-one randomized
controlled trials (RCTs) found out increased dietary calcium/dairy products, with and without
vitamin D, significantly increases total body and lumbar spine BMC in children with low
base-line intakes [73]. However, another systematic review reported no evidence to support
the use of calcium supplementation as a public health intervention to reduce weight gain or
body fat in healthy children [88].
Calcium is present in many foods, but is most concentrated in dairy products. Although
lactose intolerance can be a barrier to milk consumption among Asians, studies have shown
that subjects with lactose intolerance can consume milk and dairy foods without developing
symptoms, if amounts are divided into smaller doses throughout the day [12, 101]. It was
reported that dairy-rich diets up to 1500 mg/day of calcium can be consumed by lactose
maldigesters without significant symptoms [102]. A recent study comparing calcium intake
and bone mass between children with (n=47) and without (n=29) lactose malabsorption
reported no statistically significant difference between the groups with respect to the intake of
total calcium, milk calcium, milk, cheese, yogurt, ice cream, and calcium density of the diet
[103]. The American Academy of Pediatrics Committee on Nutrition has stated that milk and
dairy-product avoidance has a negative effect on calcium and vitamin D intake in infants,
children, and adolescents. Other nutrients such as protein make dairy products an important
source of nutrition for growing children [104]. Therefore, it is important to encourage all
Asian children, have lactose intolerance or not, to take dairy products as a primary
determinant of calcium intake.
For those who avoid cow milk protein or lactose or low-lactose milks, other available
calcium sources should be considered [6]. Some common Asian foods have been identified as
containing an appreciable amount of calcium. Non-dairy foods such as tofu, tempeh, sea
weeds, nuts and seeds dishes and green leafy vegetables etc. have been tested for calcium
bioavailability in human studies. Low-oxalate greens (eg, bok choy, broccoli, Chinese
cabbage, collards, and kale) and fruit juices fortified with calcium citrate or malate are good
sources of highly bioavailable calcium, while calcium-set tofu have good bioavailability of
calcium, and foods rich in oxalic acid (eg spinach, rhubarb, beans) or phytic acid (seeds, nuts,
grains, certain raw beans and soy isolates) have a lower bioavailability [105]. Compared to
milk, calcium absorption from dried beans is about 50% and from spinach, 10% [2]. The
calcium absorption is equivalent for soymilk and cow’s milk at similar calcium loads, if the
soymilk is fortified with calcium carbonate, not tricalcium phosphate which have lower
calcium bioavailability [106].
Conclusion
Breastmilk provides adequate calcium to meet the needs of all full-term infants. There is
no need to recommend giving calcium supplements to infants who are exclusively breastfed
or formula fed. Achieving adequate calcium is important in maximizing bone accretion
during growth, preventing child rickets, and perhaps preventing fragility fractures in
childhood or even preventing future osteoporosis. For all weaning infants and young children,
calcium intake from calcium-rich foods especially from dietary sources should be encouraged
at home, schools, and by parents, paediatricians, dietitians and by other health professionals.
Current evidence from recent studies does not support the general use of calcium
supplementation in healthy young children as a public health intervention. However, given
that infancy and childhood are critical periods for the acquisition of bone mass, if adequate
calcium cannot be achieved through food sources, supplementation is a useful alternative.
More studies related to the clinical effectiveness and/or safety of dietary supplements in
infants and children are required, especially over the longer term. Because little data are
available in this area, we suggest that parents exercise caution when giving their infants or
young children dietary supplements. Before providing dietary supplements for them, parents
should communicate with health professionals, such as pediatric doctors or dietitians.
Wherever possible it is preferable to achieve nutrient intakes, including calcium from a varied
diet rather than from supplements.
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Chapter III
Exposure of Slovenian Preschool

Children to Preservatives and
Polyphosphates
Elizabeta Mičović, Mario Gorenjak, Gorazd Meško

and Avrelija Cencič
1
Ministry of Agriculture and Environment of Republic of Slovenia in Food Safety
Directorate, Food and Feed Safety Area and Consumer Protection
2
Faculty of Medicine, University of Maribor
and Junior Researcher at Faculty of Agriculture and Life Science,
University of Maribor, Slovenia
3
Professor of Criminology and Dean at the Faculty of Criminal Justice and Security,
4
Head of the Department of Microbiology, Biochemistry,
Molecular Biology and Biotechnology at the Faculty of Agriculture and Life Sciences,
Abstract
The purpose of this paper is to present exposure of preschool children to daily
consumed food preservatives and polyphosphates: sorbic acid, benzoic acid, nitrate,
nitrite, sulphur dioxide and polyphosphates. For exact exposure of chemicals in food,
data of consumed food intake and concentration of observed chemicals in food are
needed. Methodology: Among the randomly selected regions in Slovenia, we randomly
selected kindergartens and children aged from 2-6 years. The study included 190
children, 98 boys and 92 girls. Anthropometric measurements of children were
conducted, so data on the sex, age, measured weight and height of the children were
available. The dietary intake was based on the 3-day-weighed record method. The data
from databases obtained from the official control and monitoring of food additive content

Contact: elizabeta.micovic@gmail.com.
68 Elizabeta Mičović, Mario Gorenjak, Gorazd Meško et al.
in consumed food were used to calculate estimated daily intake (EDI). Such estimated
exposure of each preservative and polyphosphates EDI was compared with acceptable
daily intake (ADI) and expressed as % of ADI. Results: average exposure to each
preservative and polyphosphates EDI was not exceeding ADI. It is evident that average
exposure to nitrites and sulphur dioxide is relatively high, while intake of benzoic acid,
sorbic acid, nitrates and polyphosphates is not so high. The mean daily exposure of
children to nitrites ranged from 12.8 % to 28.3 % ADI, to sulphur dioxide from 14.3 % to
21.4 % ADI, while to sorbic acid from 3.8 % to 4.5 % ADI and polyphosphates from 1.8
% to 3.9 % ADI.
It is apparent that such exposure does not present any harm or threat to observed
children although we should consider the fact that ADI for sum of preservatives and
polyphosphates have not been set yet.
Keywords: Preschool children, exposure, preservatives, polyphosphates, ADI
1. Introduction
Environmental factors play a major role in determining the health and well-being of
children. Accumulating evidence indicates that children, who comprise over one third of the
world’s population, are among the most vulnerable of the world’s population and that
environmental factors can affect children’s health quite differently from adults’ health (WHO
2006). One of the most important environmental factors, which have strong impact on
children health, is food. Children have different susceptibilities towards food during their
different life stages, giving their dynamic growth and developmental processes as well as
physiological, metabolic, and behavioural differences. Children consume more food and
beverages per kilogram of body weight than adults do. Also their dietary patterns are different
and often less variable during different developmental stages. Children’s metabolic pathways
may differ from those of adults. They have more years of future life and thus more time to
develop chronic diseases that take decades to appear and that may be triggered by early
environmental exposures. They are often unaware of environmental risks and generally have
no voice in decision-making. The accumulating knowledge that children may be at increased
risk at different developmental stages, with respect to both biological susceptibility and
exposure, has raised awareness that new risk assessment approaches may be necessary in
order to adequately protect children. Traditional risk assessment approaches and
environmental health policies have focused mainly on adults and adult exposure patterns,
utilizing data from adult humans or adult animals. There is a need to expand risk assessment
paradigms to evaluate exposures relevant to children from preconception to adolescence,
taking into account the specific susceptibilities at each developmental stage. The full
spectrum of effects from childhood exposures cannot be predicted from adult data. Risk
assessment approaches for exposures in children must be linked to life stages (WHO 2006).
Almost in all food categories, preservatives are added to ensure longer shelf life of food
products. It is very important that only proven preservatives can be used by food producers, in
certain food product and in allowed quantities. Exposure to each preservative must not exceed
acceptable daily intake (ADI), the amount of the substance considered to be safely consumed,
daily, throughout a lifetime. This assessment is used to set the maximum amount of a
particular additive permitted in a specific food, either as a specified number of grams or
Exposure of Slovenian Preschool Children to Preservatives ... 69
milligrams per kilogram or liter of the food or, if the ADI is very high or “non-specified”, at
quantum satis - as much as is needed to achieve the required technological effect, according
to good manufacturing practice. To ensure that consumers are not exceeding the ADI by
consuming too much of, or too many products containing a particular additive, the EU
legislation requires that intake studies be carried out to assess any changes in consumption
patterns (Emerton and Choi 2008).
The vast majority of toxicity studies and risk evaluations deal with single preservatives
and single chemical. In reality, humans are exposed to large numbers of chemicals via
multiple routes (Feron and Groten 2002; Feron et al 2002; Groten et al. 2004). So far,
possible effect of mixture of all chemicals and interactions between them, so called ’cocktail
effect’, have not been understood fully. Food additives are typically used in combination
within processed foods and therefore collectively may have some adverse effects at the
cellular level, even if their individual concentrations are below the ADI value (Lau et al.
2005).
2. Consumer as Possible Victim of Invisible

Threats
“Consumers by definition, include us all. They are the largest economic group, affecting
and affected by almost every public and private economic decision. Furthermore, consumers
are the only important group whose views are often not heard” (Kennedy 1962). Consumer is
a person who buys goods or services for personal needs and not for resale or use in the
production of other goods for resale (Consumer protection Act, 2004).
Consumers expect a wide range of competitively priced, highly processed and convenient
food products of consistently high quality. They expect it to be fresh, good looking,
nutritious, wholesome, tasty and it must be primarily and absolutely safe. On the other hand,
consumers have no direct means for the verification of their expectancies and have to rely
completely on the food legislators and enforcement agencies (Anklam and Battaglia 2001).
Consumers could be victims of food poisoning, food adulteration and food frauds, misleading
regarding food content (labelling), misleading indications, misleading descriptions,
misleading pictures, food packaging (Jin and Kato 2004; Gibson and Taylor 2005; Tombs
2008; Croall 2009).
In today’s technological age, a reactive response to the consumer fraud is neither efficient
nor effective (Holtfreter et al. 2005).
Consumers are privileged to have human rights. However, they come with certain
responsibilities too - to seek, to evaluate and to use available information on products and
services, to make healthier and better decisions for themselves and for their children. In case
of exposure to different chemicals in food, consumers know that food product consist
additives, but they do not know the quantity of them.
Total intake is unknown, so how could parents be sure that the consumed food is safe for
their children? It is very important to consider different sensitivity of population, especially
among infants and children.
3. Food Safety
The main challenge in the area of agriculture is to provide sufficient quantities of food,
which have to be of good quality and safe. Food production and food consumption are the
primary aspects of our lives and are therefore subject to our care. To achieve these goals
agriculture and food industry have to use in their production different chemicals such as
pesticides and food additives. Without the use of chemicals the yields of fields will reduce,
food production and the earnings will be considerably smaller. While with using chemicals
the benefits are visible, the risks are often invisible, even they effects on us and make us
vulnerable (Beck 2001). Safe food is food that is free from not only toxins, pesticides,
chemical and physical contaminants, but also from microbiological pathogens such as
bacteria and viruses that can cause illness (Golob and Jamnik 2004).
There are main concerns regarding food safety. Consuming food is daily routine activity
throughout lifetime. It is very important that such food does not cause health risk to
consumer. Possible hazards in food are microorganisms, viruses, contaminants (toxins, heavy
metals), pesticides and other chemicals. Consumer could be concerned and afraid of such
hazards, but in many cases one does not know exact quantity of exposure and exact effect on
his health. Therefore, it is very important to be aware of possibility of invisible threats in
food. Food industry has a strong motive to make profit and many opportunities to manage it.
Food operators try to convince consumers that they need their products, so they use all sorts
of food additives, ingredients and advertising tactics to achieve better sale (Cheftel 2005).
Consumers have the legal right to be protected (Xu and Yuan 2009). The long-term
health of consumers are also endangered by the use of foods and other consumer products of a
vast range of chemicals and other substances that, while associated with long- term health
risks, do not result in immediate harm. While there is a growing public concern about the
number of foods and consumer issues, these facts have a lower political and governmental
profile than the occupational health and safety or the safety of the environment (Croall 2009).
The main authority concerns, regarding food safety, are to protect interests of public
health, interests of food producers (economic view) and the consumer interests and their
rights. It is not easy to make right decision and to achieve all that goals in practice at the same
time. Recognizing possible invisible threats could assure better consumer protection.
Furthermore, knowing all the risks of invisible threats in the food area help us to make
corrective measures on time.
These measures could make system for food safety more effective and give consumers
better protection. The big challenge in the area of food safety for consumer health is
recognition of possible invisible threats on time. This can help us to set up effective response
regarding those threats and risk assessment. Identifying all potential hazards that have to be
assessed, eliminating or reducing them to acceptable levels, are the most important activities
for achieving consumer protection, specially their basic right to safety (Mičović 2010).
3.1. Risk Analysis
Public health decisions on the plausible risks of chemical exposures can include several
possible outcomes. The ultimate goal is to implement a risk management action that will
produce the desired reduction of risk. A risk analysis paradigm is a formal representation of a
process that distinguishes the scientific bases from the risk management objectives and
generally contains a component where the probability of harm is estimated.
The overall risk analysis process includes risk assessment, risk management and risk
communication, and involves political, social economic and technical considerations.
Moreover, there is consensus among scientists that risk assessment should be an independent
scientific process, distinct from measures taken to control and manage the risk. Risk assessors
are responsible for scientific evaluation whether a formal risk assessment is necessary or not
(Benford 2001). As a probability calculation, a risk assessment will include both a statement
of the objective under consideration (harm) and the basis for the assertion that the harm may
occur (probability). Risk management is the decision-making process involving the
consideration of political, social, economic and technical factors with relevant risk assessment
information relating to a hazard so as to develop, analyze, select and implement appropriate
risk mitigation options. Risk management comprises of three elements: risk evaluation,
emission and exposure control and risk monitoring (WHO 2004).
Risk management strategies may be regulatory, advisory or technological and take into
account factors such as the size of the exposed population, resources required and available,
costs of implementation and the scientific quality and certainty of the risk assessment.
Risk managers are responsible for judgments concerning the acceptability of risk; they
have to weigh risk against other factors including costs, benefit and social values, so called
risk – benefit approach. Risk communication should include interactive exchange of
information and opinions among risk assessors, risk managers, consumers and all other
interested parties, often called stakeholders (Benford 2001).
3.1.1. Risk Assessment

The procedures used to estimate exposure to chemicals contaminants in food are
essentially the same as those used for food additives (DiNovi and Kuznesof 2006). Exposure
assessment should cover the general population, as well as critical groups that are vulnerable
or are expected to have exposures that are significantly different from those of the general
population, for example infants, children, pregnant women, or the elderly (WHO 2005).
Risk is defined as the chance or probability of an adverse health effect occurring and
severity of that effect (Benford 2001). Risk assessment is a scientific process, conducted by
scientific experts, who may begin with a statement of purpose intended to define the reasons
that the risk assessment is required and support the aims of the subsequent stages of risk
management. Chemical risk assessment often does not have a formal statement of purpose
(Benford 2001). Generally, formal risk assessments are preceded by preliminary risk
assessments. These are usually subjective and informal and may be initiated from inside or
outside the risk assessment and scientific communities. A key consideration of these
preliminary risk assessments is whether a formal risk assessment is necessary or not (WHO
2004). However, risk assessment may be defined implicitly in a generic form, as in the terms
of reference of an expert committee, such as Joint FAO/WHO or JECFA. In this context, it
concerns the definition of acceptable or tolerable levels of intake for a chemical in food that
may require review and revision in the light of new information. It is very important fact, that
risk assessment may need to be quantified differently for persons with different degrees of
susceptibility. Risk assessment for chemical agents requires consideration of the factors
mentioned before and these are generally encompassed within the stages of the overall risk
assessment process, defined as hazard identification, hazard characterization, and exposure

assessment risk-characterization (Benford 2001).
Hazard identification is the process of identification of the type and nature of adverse
health effects (human studies-epidemiology, animal – based toxicology studies, in- vitro
toxicology studies, structure-activity studies (cell cultures, tissue slices). Hazard
characterization involves the derivation of a level of exposure at or below which there would
be no appreciable risk to health if the chemicals were to be consumed daily throughout life.
Exposure assessment is evaluation of concentration or amount of a particular agent that
reaches a target population: magnitude, frequency, duration, route, extent.
Risk characterization is the stage of risk assessment that integrates information from
exposure assessment and risk characterization into advice suitable for use in decision-making
(Benford 2001).
The basic concept underlying any chemical risk assessment is the dose-response
relationship. As described by Paracelsus nearly 500 years ago, “All substances are poisons;
there is none which is not a poison. The right dose differentiates a poison and a remedy”
(Winter and Francis 1997). This means that any chemical substance is likely to produce some
form(s) of harmful effect, if taken in sufficient quantity. Experts refer to a potential harmful
effect as a hazard associated with that substance. The definition of hazard is “a biological,
chemical or physical agent with the potential to cause an adverse health effect” (Unnevehr
2003; Raspor, 2004; Armstrong 2009). Whilst this may be appropriate with respect to
pathogenic organisms, chemical substances may be associated with a number of different
adverse health effects, not all of which would necessarily be expressed in a specific exposure
scenario. Therefore, experts dealing with chemical substances prefer to define the potential
health effects as individual hazards which need to be considered separately during the
evaluation. The likelihood or risk of that hazard actually occurring in humans is dependent
upon the quantity of chemical encountered or taken into the body, i.e. the exposure. The
hazard is an inherent property of a chemical substance, but if there is no exposure, then there
is no risk that anyone will suffer because of that hazard.
Risk assessment is the process of determining whether a particular hazard will be
expressed at a given exposure level, duration and timing within the life cycle, and if so the
magnitude of any risk is estimated (Benford 2001). Among the first objectives of a risk
assessment is the determination of the presence or absence of a cause-effect relationship. If
there is sufficient plausibility for the presence of such a relationship, then dose - response
modelling (DRM) information is needed.
3.1.2. Acceptable Daily Intake (ADI) and Estimated Daily Intake (EDI) of
Food Additives
The concept of the ADI, is internationally accepted today as the basis for estimation of
safety of food additives and pesticides, for evaluation of contaminants and by this, for
legislation in the area of food and drinking water. The ADI (Chart 1) is an estimate of the
amount of a food additive, expressed on a body weight basis that can be ingested daily over a
lifetime without appreciable health risk (WHO 1987). Although, ADI has derived from the
safety assessment of each food additive, their combined adverse effects are unclear and have
not been widely studied. Food additives are typically used in combination within processed
foods and therefore, collectively may have some adverse effects at the cellular level, even if
their individual concentrations are below the recommended ADI value (Lau et al. 2005).
Dose response modelling (DRM), used as quantitative risk assessment tool for public
health recommendations about chemical exposures, can be described as a six-step process.
The first four steps—data selection, model selection, statistical analyses, and parameter
estimation—constitute dose–response analysis. The fifth step involves the integration of the
results of the dose–response analysis with estimates of human exposure. The final step
involves an assessment of the quality of the dose–response analysis and the sensitivity of
model predictions to the assumptions used in the analysis.
Chart 1. Acceptable daily intake of preservatives and polyphosphates
Preservatives E number ADI (mg/kg BW/day)

Sorbic acid E 200 0-25 (JECFA*, 1973)
Benzoic acid E 210 0-5 (JECFA, 2002)
Nitrate E 251 0-3.7 (SCF**; JECFA 2002)
Nitrite E 250 0-0.07 (JECFA, 2002)
Sulphur dioxide E 220 0-0.7(JECFA, 1973)
Polyphosphates (E 450-452) 0-70(JECFA, 1981-2001)
*, **Acceptable daily intakes have been derived from toxicological studies by the former EU Scientific
Committee on Food (SCF) and by the WHO/FAO Joint Expert Committee on Food Additives and
Contaminants
Extrapolation is a fundamental problem in the quantitative health risk assessment of

exposure to chemicals that are toxic to human in experimental systems. Adverse health effects
of chemicals are, in the absence of human data, typically evaluated in laboratory animals at
significantly higher doses than the levels to which humans may be exposed. Moreover, the
data obtained in animals are very often misleading, as the animals used usually do not
respond to the toxic compounds in the same way as humans (WHO 2004).
The acceptable daily intake (ADI) is used widely to describe “safe” levels of intake; other
terms that are used are the reference dose (RfD) and tolerable intakes that are expressed on
either a daily (TDI or tolerable daily intake) or weekly basis. The weekly designation is used
to stress the importance of limiting intake over a period of time for such substances (Herman
and Younes 1999).
In order to calculate an ADI using the data from toxicity studies, the lowest dose should
ideally result in no effects under the conditions of the particular study. That dose may be
termed as the No Observed Effect Level (NOEL). Observed effects are referred to
assumptions and can not be made regarding effects not detectable by the methods used.
Some effects observed in toxicity studies may represent adaptive responses with no
implications for the health status of the animal and would generally not be used as the basis
for establishing an ADI. Effects that are considered to result in harm to the animal are
referred to as “adverse”, and therefore some expert committees use the expression No
Observed Adverse Effect Level (NOAEL) (Benford 2001). When using this approach
NOAELs are identified in the critical studies, to which appropriate safety or uncertainty
factors are applied. Although the value of safety factors varies depending upon a number of
factors, 100 is most often used, which is designed to account for interspecies and interspecies
variations (Herman and Younes 1999).
ADI = NOAEL/ 100
Estimated daily intake (EDI) is value of chemical exposure, which can be determined by
combining food consumption data with data on the concentration of additives in food. The
resulting dietary exposure estimate is afterwards compared with the relevant toxicological or
nutritional reference value for the food additive concern, for example acceptable daily intake
(ADI) or tolerable daily intake (TDI) (WHO, 2005). Usually EDI is expressed as percentage
of value of ADI for each food additive.
If EDI is lower or the same as ADI, there is no concern regarding such exposure and we
can assume that food additive intake among observed population represent no risk. If EDI is
higher or the same as ADI, than exact risk assessment should be done on case-by-case base,
and risk managers should decide and take effective measurements.
3.1.3. Preservatives and Polyphosphates

For successful food production and selling food the most important are quality, safety,
shelf life and price of the food product. Quality food product is source of suitable nutrients
but it should has good taste and look, but above all it should be safe for consumption and
must not be harmful for health of consumer (Lu 1991; Renwick 1996; Emerton and Choi
2008). Additives are substances which are intentionally added to food products and are
therefore amenable to be limited or, if necessary, prohibited altogether (Huggett at al. 1998).
They are not main ingredients in food products but they are added to food with aim to
improve technological or sensory properties (look, taste, texture, longer shelf life).
The authorization of food additives should be determined food, which these additives
may be added, and the conditions under which they may be added. One principle is certain
additives permitted for each sort of food and the other is ADI for this food additive. In certain
food products, the addition of additives is prohibited (such as preservatives in dairy products)
or limited (baby food). Therefore should be precise, what allowance should be additive to
achieve the desired effect. The principle is to be tries with the lowest possible dose of
additives to achieve the desired effect. It is very important to take into account the acceptable
daily intake or other additive intake estimates and the probable daily intake from all sources.
When the additive is used in food for groups of consumers with special dietary needs should
be considered acceptable daily intake of a food additive for this group of consumers (Emerton
and Choi 2008).
Preservatives are certainly the most important group of additives, since they play an
important role in ensuring food safety. They are used to protect against food poisoning, so as
to prevent the development of microorganisms and thereby prolong the shelf life and achieve
stability of food products (Emerton and Choi 2008).
There are natural and unnatural preservatives (Simon and Ishiwata 2003) which prevent
growth of bacteria, fungi and viruses and thus prevent food from spoilage.
While food preservatives can increase stability of food, polyphosphates give certain
product sensory properties (taste, mouth feel and texture). Thus, there are also
polyphosphates, which are added to the meat industry in a variety of products in order to
make the meat retained more water you add to food products according to a recipe. The
production of meat products phosphate additives primarily use to an increase in binding of
water, which naturally improves the taste. In cooked meat products and precipitated such
added 0.1% to 0.5% polyphosphate (Emerton and Choi 2008; Uribari 2009).
In addition to the meat industry, where polyphosphates represent one of the key
technological elements of the food additives used in the manufacture of cheeses, bakery
products and a variety of drinks. Some studies linking intake of preservatives to the
occurrence of allergic reaction, food intolerance and urticaria (Yang and Purchase 1985;
Hannuskela and Haahtela 1987; Schultz-Ehrenburg and Gilde 1987; Steinman, Le Roux and
Potter 1993; Hawkins and Katelaris 2000; Merget and Korn 2005, Andersson, Knutsson,
Hagberg, Nilsson, Karlsson, Alfredsson and Torén 2006; Michaëlsson and Juhlin 2006), so it
is very important to find out exact exposure to food additives.
4. Study among Preschool Children in Slovenia

The purpose of research was to assess if preservatives and polyphosphates intake could
be possible threat to the health of preschool children. It is assumed that intake of each food
additive separately could not be so high or greater than ADI. However, it is unknown the total
intake of all food additives per day. It is assumed that higher exposure to food additives is in
relation to appearance with possible harm reactions among observed children. In the first
place, it is necessary to find out the exact quantity of consumed food and then exposure to
food additives, in our case preservatives and polyphosphates, added to food.
4.1. Methodology
4.1.1. Observed Population

Among by randomly selected regions in Slovenia, we selected kindergartens and all
children aged 2-6 years. Initially, the study included 250 children, representing all children of
one section of selected kindergartens. Due to incomplete data, 60 children were excluded
from observation. Therefore, the total number of children used in this study were 190, 98
boys and 92 girls. Anthropometric measurements of experimental children groups were
conducted as for example data regarding their age and gender, weight and height. In the
selected group, Boys and girls were divided into two groups regarding their age: 2-3.9 years
and 3.9-6 years.
4.1.2. Food Consumption Data

The dietary intake is generally based on the 3-day-weighed record method in the
kindergartens and homes. In the kindergartens subject to the research, we have weighed
quantities of individual foods and dishes, randomly chosen and offered to the observed
children. Quantity of food eaten by children at home, were collected by questionnaire, which
were answered by parents.
Data were calculated by average day and body weight of each child included into
research.
Food intake (g) = food offered (g) - waste food on the plate (g)
From these data, we have obtained the exact amount of food eaten by each child in three
days. Specific types of food it has divided regarding to their characteristics in the following
categories as shown Chart 2. It was considered those food categories in a particular food or
otherwise adds any additives, which are the subject of our research. These are mainly
processed industrially prepared food.
Chart 2. Food categories included to study
Food category Food product

Non-alcoholic beverages coca-cola, ice-tea
Fat spreads margarine, butter
Bakery products bread, cookies, pastry
Fruit products dried fruits, jams, candied fruits
Confectionary products chocolate like products, cream cakes, milk cakes
Meat products salami, pate, hot-dogs
Snacks salty snacks
4.1.3. Estimated Daily Intake of Preservatives and Polyphosphates (EDI)

Additives included in the research are preservatives: sorbic acid (E 200), benzoic acid (E
210), nitrate (E 251), nitrite (E 250), and emulsifiers: polyphosphates (E 450-452);
To estimate the daily intake of preservatives and polyphosphates we had to combine food
consumption data with data on the concentration of observed additives in food.
EDI = food additive concentration x food consumption per body weight
Calculation of the average daily consumption of specific groups of food per body weight
for each child was made. The data from databases obtained from the official control and
monitoring on food additives content in different food categories were used. To calculate how
much of each additive, the children daily ingested per kg body weight, food additives were
added together, equal and shared with the child's body weight expressed in kg and thus
received the additive value in mg/kg body weight.
4.1.4. Comparison between ADI and EDI

To assess safety of food additives exposure, ADI of each food additive have been carried
out. The estimated daily intake (EDI) of each additive is acceptable and safe if its value is
lower or the same as ADI. To determine safety assessment among observed children
regarding exposure to preservatives and polyphosphates, EDI was compared with ADI, and
expressed in percentage of ADI.
5. Results
5.1. Characteristic of Observed Sample
The study included 250 preschool children, but, as shown in Chart 3, we have 60
excluded from consideration. The reason for this was that in the absence of some children in
kindergarten at the time of carrying out research or incomplete information on foods eaten at
home, provided by the parents. That was the deal involved only 190 children, 98 boys and 92
girls aged 2 to 6 years. The population of children was divided into two age groups: 2 to 3.9
years and 4-6 years, were divided by gender: girls (F) and boys (M). In the first age group
was 31 boys and 20 girls in the second age group was 67 boys and 72 girls. The average body
weight of each considered children in the first group of boys was 16.86 kg ± 1.74 kg and
among girls 14.95 kg ± 1.44 kg. In other age group, average weight was 20.61 kg ± 4.03 kg
among boys, and 19.60 kg ± 2.96 kg among girls.
Chart 3. Observed population
No. of Avg. body

Group Gender Standard deviation
children weight (Kg)
M 31 16.86 1.74
2-3,9 y
F 20 14.95 1.44
4-6 y M 67 20.61 4.03
F 72 19.60 2.96
5.2. Food Consumption Data
Weighing three-day method was used to determine the food intake data among observed
children in kindergarten. Quantity of food eaten by children at home, were collected by
questionnaire, which were answered by parents. Consumed food were classified into food
categories shown in Chart 2, and calculated the average intake of each food category. We
performed the anthropometric measurements of observed children, and take into account body
weight to calculate the intake of food per kilogram of body weight of each child. Chart 4
therefore shows the average daily intake of all consumed food in three days, expressed in
grams per kg body weight (g/kg BW). In the first age group boys consumed significantly
more food than girls. In another age group 4-6 years, the difference in quantity of consumed
food among girls and boys is not so relevant. Regarding the above results, it is interesting fact
that the intake per kilogram of body weight is higher among smaller and younger children.
This is very important regarding of risk assessment and set the acceptable daily intake of
additive. In case of the same amount of consumed food is exposure to food additives for
lighter child higher than exposure to equal quantity of additives for child with higher body
weight.
Figure 1 shows the average intake of food categories among observed children. It is clear
that children consume most bakery products and dairy products, which is understandable.
Bakery products and milk products are basic foodstuffs included in a daily nutrition of
preschool children and include bread, breakfast cereals, cereal grains, cereals, milk and
yogurt. Compared to other food it is obviously that quite large intake of consumed food
belongs to confectionery products, such as sweets, chocolate, chocolate-like products,
lollipops, chewing gums and meat products such as salami, hot dogs and pate.
Chart 4. Average daily intake of all consumed food
Standard deviation
Average daily Average intake
Group Gender of average daily
intake (g) (g/kg BW)
intake
M 350.63 83.19 20.79
2-3.9 y
F 318.51 65.05 21.30
M 336.82 61.79 16.34

4-6 y
F 330.61 65.51 16.86
Figure 1. Average intake of food category among observed children.
These products are very popular among children and they like them. Among older
children we noticed increasing of consumed fat spreads, bakery products, fruit products,
confectionery, meat products and snacks and decreasing intake of dairy products. This is
logical, because parents offer dairy products in the meals more often to younger children.
Relatively high quantity soft drinks (1.79 ± 5.44 g/kg BW) were consumed by girls aged 2 to
3.9 years, which is clearly shown in Figure 1. Category of fat spreads and dairy products were
excluded from further analysis because the observed preservatives and polyphosphates were
not having been identified in official control in these categories of food.
5.3. Estimated Daily Intake of Food Additives
Levels of preservatives and polyphosphates in different food products are known from
official inspections and analysis reports on content of food additives in different food
products. Food products were set in food categories shown in Chart 2 and Figure 1. The
results show that preservatives are added into bakery products (sorbic acid and benzoic acid),
non-alcoholic beverages (sorbic acid and benzoic acid), fruit products (sulphur dioxide) and
meat products (nitrites, nitrates, and polyphosphates). From results of analysis reports, we can
calculate exact quantity of preservatives and polyphosphates added in consumed food. As
Chart 5 shows, the higher intake of preservatives and polyphosphates expressed in mg/kg
body weight, are among older children, 4-6 years old girls. It is very interesting, that the
highest daily intake of preservatives and polyphosphates belongs to polyphosphates,
commonly added to meat products.
Chart 5. Average intake of preservatives and polyphosphates (mg/kg BW)
Polypho
Benzoic Sorbic SO2 Nitrites Nitrates
sphates
Group acid acid TOTAL SD
mg/kg mg/kg mg/Kg mg/Kg mg/Kg
mg/Kg/BW
BW BW BW BW BW
2-3.9 years
0.024 1.022 0.126 1.368 0.01 0.027 2.577 0.60
old M
2-3.9 years
0.122 1.13 0.1 1.242 0.009 0.024 2.627 0.58
old F
4-6 years old
0.065 1.008 0.127 2.106 0.015 0.041 3.362 0.85
M
4-6 years old
0.032 0.945 0.15 2.735 0.02 0.053 3.935 1.08
F
TOTAL 0.243 4.105 0.503 7.451 0.054 0.145
SD 0.04 0.08 0.02 0.70 0.01 0.01
Figure 2. Average intake of benzoic acid.

Figure 3. Average intake of sorbic acid.
The average daily intake varied between 1.242 to 2.735 mg/kg BW. This fact is not so
unusual, regarding to high value of the ADI for polyphosphates (0-70mg/kg BW/day). It is
obviously that this result goes in line with quantity of consumed meat products by girls 4-6
years old. In comparison with the intakes of other preservatives is also fairly high daily intake
of sorbic acid, which is on average from 0,945 to 1,130 mg/kg BW/day. Figures 2-7 show the
average amount consumed each observed preservatives and polyphosphates among children
included in the study and it is obviously that average intakes of each preservative do not
exceed the ADI.
Figure 4. Average intake of sulphur dioxide.

Although average intakes above additives do not exceed the ADI, we have found eight
children who have been exposed to higher levels of intake than ADI, namely exposure to
sulphur dioxide, which is 1.048 to 1.930 mg/kg BW. ADI of sulphur dioxide is 0-0.7 mg/kg
BW. Estimated daily intakes of other preservatives and polyphosphates among the individual
child do not exceed the ADI.
Figure 5. Average intake of polyphosphates.
Figure 6. Average intake of nitrites.

Figure 7. Average intake of nitrates.
Figure 8. EDI–ADI relationship of preservatives and polyphosphates.

Figure 9. Average total intakes of preservatives and polyphosphates.
5.4. Results of Comparison between EDI and ADI of Preservatives and

Polyphosphates
Results of safety assessment regarding relation between EDI and ADI of preservatives
and polyphosphates show that average intake of each additive are acceptable and safe. Figure
8 presents EDI - ADI relationship of preservatives and polyphosphates.
It is evident that exposure to nitrite and sulphur dioxide is relatively high, the highest
among older children. Intake of benzoic acid, sorbic acid, nitrates and polyphosphates is not
so high. It is interesting that EDI to sulphur dioxide and nitrite is relatively high in compare to
other preservatives and polyphosphates, and it is in range 14.3 to 21.4 % ADI for sulphur
dioxide and 21.4 to 28.3 % ADI for nitrite. It could be concluded that basic food products that
are consumed very often by children (few times a day) contain sulphur dioxide and nitrites.
Such food products are fruit products and meat products.
5.5. Results of Total Intake of Preservatives and Polyphosphates
Although average intake of each preservative and polyphosphates do not exceed ADI and
we can conclude that such exposure is acceptable and safe, we wonder about exposure of total
intake - preservatives and polyphosphates together. We calculated sums of intakes of all
observed preservatives and polyphosphates and we expressed them for each group of children
in Figure 9.
Results show that sum of total intake of preservatives and polyphosphates for each group
of children is in range from 2.63 to 3.36 mg/kg BW. Total intake is higher among older
children, especially among girls from 4-6 years old. Unfortunately we cannot compare these
intakes with any ADI, because ADI for mixtures of additives have not been set yet. Anyway,
values in consideration with average children’s body weight tell us enough for themselves.
Conclusion
The human health risk assessment of food constituents is an internationally agreed and
well-established process, being an integral part of the risk analysis process, which also
includes risk management and risk communication. These three elements are separate tasks,
performed by different players, however each of them is very important. With exchanging
knowledge and cooperation, they are parts of an interactive process.
The risk assessment of chemicals in food is a purely scientific process that requires
expertise in toxicology, nutrition and exposure assessment.
The risk management includes an identification of the food safety problem, consideration
of its magnitude, seriousness, and consequently the way of handling it. In this process, the
risk manager may include cost-benefit considerations before deciding how to manage the case
(ban the compound, introduce limitations, provide specific dietary advice or accept the status
quo). Finally, the risk analysis must include a clear and interactive risk communication with
consumers, food industry and other stakeholders. In this study an example of risk assessment
is presented, special exposure assessment of preservatives and polyphosphates among
preschool children in Slovenia. Ultimately 190 children attending kindergarten (of which 92
girls and 98 boys aged 2-6 years) took part in the study. The results showed that nutrition
regarding the quantity of food consumed among Slovenian preschool children does not differ
between regions in Slovenia.
It is obvious that people responsible for preparing meals in kindergartens follow the
guidelines for healthy nutrition recommended by Ministry of Health of Republic of Slovenia.
Food habit questionnaires answered by parents of children participants at home showed a big
difference between children nutrition in kindergartens and that at home.
The observation of individual child included in the study showed the differences in
pattern of food consumption at home. Parents have very different levels of knowledge
regarding ingredients included in food products, healthy nutrition and possible effect of food
additives on children health. Some of them are aware of the importance of healthy balanced
diet and nutrition.
They offer their children food products without food additives, or they rarely offer them
processed foods containing additives in relatively small quantities.. They also combine meals
at home with food that has not been eaten in the kindergarten. However, there are some
parents, who do not pay attention to food included into meals at home and composition of
meals in kindergarten. The study’s results show, that their children were exposed to higher
level of preservatives and polyphosphates. It is apparent that such exposure does not present
any harm or threat to observed children, regarding comparison between estimated daily intake
(EDI) and acceptable daily intake (ADI) of each food additive.
The other very important problem is the total intake of all food additives daily consumed
by children: preservatives, polyphosphates, sweeteners and colours together. The fact is that
ADI for sum of food additives has not been set yet. According to the study’s results, exposure
to preservatives and polyphosphates is relatively high among observed children. We must not
forget that children consume also other food additives, such as colours and sweeteners.
We strongly believe that future study should lead to exposure assessments of mixture of
chemicals and interactive influence among them. We must not forget that children are
vulnerable and the most sensitive part of the population and could become victims of invisible
threats.
Parents and their children as consumers have the right to safety, the right to be informed
and the right to choose. We should put more attention to educate parents to become aware of
importance of possible effects of nutrition on health of their children. They should combine
meals for their children in a way to achieve as lower exposure to food additives as possible.
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Chapter IV
The Breakfast Experience in Low

Socioeconomic Families with
Overweight Children
Simone Pettigrew* and Melanie Pescud†

University of Western Australia
Abstract
Dietitians emphasise the importance of a healthy breakfast as part of a balanced diet.
As well as providing energy to fuel physical and mental activity, there is increasing
evidence that eating breakfast assists individuals manage their food intake to prevent
excessive weight gain. Parents play a critical role in determining if their children eat
breakfast and, if so, the kinds of foods that are consumed at this meal. Limited previous
research has specifically examined parents’ beliefs and behaviours in relation to this
aspect of their children’s diets. Such information is especially important in the context of
low socioeconomic families given that disadvantaged children have significantly higher
rates of overweight and obesity and poorer academic performance relative to their more
advantaged peers. In the present study, parents’ attitudes to breakfast and its role in
children’s health were explored. A range of qualitative data collection methods was
employed over an extended period (12 months) with low socioeconomic status parents of
overweight children. Insights were generated into the barriers, motivators, and facilitators
influencing whether parents provide their children with healthy breakfasts. Numerous
factors were listed as making it difficult to ensure children eat a healthy breakfast. These
included time constraints, children’s taste preferences, a lack of appetite upon waking,
and a reluctance among some parents to model recommended breakfast consumption
behaviours. The findings indicate that future efforts to improve children’s nutrition could
(i) build on parents’ existing belief that breakfast is important and (ii) suggest coping
* Professor Simone Pettigrew, Business School, University of Western Australia Ph: +61 8 6488 1437
simone.pettigrew@uwa.edu.au.
†
Melanie Pescud, Business School, University of Western Australia Ph: +61 8 6488 2972
melanie.pescud@uwa.edu.au.
90 Simone Pettigrew and Melanie Pescud
strategies for parents to overcome the identified barriers to selecting and serving healthy
breakfast foods.
Introduction
Child obesity is a common affliction across the developed world (World Health
Organization, 2010). In Australia, the context of the present study, one in four children is
either overweight or obese (Australian Bureau Statistics (ABS), 2009). The rates vary by
socioeconomic status (SES), with one in three low SES children being overweight or obese
compared to one in five high SES children (ABS, 2009).
Numerous factors that are contributing to the obesity epidemic have been identified.
These include escalating food marketing (Nestle, 2006; World Health Organization, 2006;
Zimmerman, 2011), more food being consumed outside the home (Burns et al., 2002), the
introduction of trans fats and high fructose sugars into the food supply (Lichtenstein et al.,
2006), and a growing proportion of two-income households in which there is less time for
food preparation (ABS, 2000). Each of these factors places upwards pressure on the amount
of energy consumed by individuals.
Energy is consumed during meals and when consuming snacks (Nielsen et al., 2002),
with snacking in particular being likely to involve highly energy-dense foods (Lipsky, 2009).
As a result, considerable previous research has focused on the extent to which snack foods
and other high energy density foods are promoted to and consumed by children (Cairns et al.,
2009; Piernas and Popkin, 2010). In recent years, other eating occasions have attracted
increasing attention in efforts to develop a more comprehensive approach to preventing and
treating child obesity. For example, in recognition of the importance of breakfast for
children’s nutrient intake (Affenito, 2007; Williams, 2007), various studies have assessed the
extent of breakfast skipping among children (e.g., Barton et al., 2005; Cheng et al., 2008;
Deshmukh-Taskar et al., 2010; Delva et al., 2006; Dubois et al., 2006; Sampson et al., 1995;
Shaw 1998; Tin et al., 2011; Vanelli et al., 2005). These studies have concluded that skipping
is quite common, resulting in calls to develop and implement intervention strategies designed
to encourage breakfast consumption among children (Dubois et al., 2006; Pearson et al.,
2009; Rampersaud et al., 2005). However, there has been a lack of research into the reasons
for children’s breakfast skipping behaviours to inform such interventions.
The present study seeks to generate insight into Australian children’s breakfast-related
behaviours by gathering qualitative data from low socioeconomic parents of overweight
children over an extended time period. The rationale for this sample and the methodological
approach adopted are explained after the following review of relevant literature.
Literature Review
Breakfast has long been held by conventional wisdom to be an important part of the
overall diet. Hence pioneer nutritionist Adelle Davis’ famous quote, “Eat breakfast like a
king, lunch like a prince, and dinner like a pauper” (Rattiner, 2002, p.1). In terms of child
obesity, cross-sectional studies usually demonstrate an inverse relationship between
The Breakfast Experience in Low Socioeconomic Families … 91
frequency of breakfast consumption and body mass index (Affenito, 2007; Deshmukh-Taskar
et al., 2010; Szajewska and Ruszczynski, 2010; Thompson-McCormick et al., 2010; Tin et
al., 2011; Utter et al., 2007; Williams, 2007). Body mass index (BMI) is calculated by
dividing weight by height squared (Lobstein et al., 2004), and provides a robust indication of
weight status (i.e., whether an individual is underweight, normal weight, overweight, or
obese) (Bouchard, 2007). The tendency for breakfast consumption to be associated with lower
BMI holds despite a typically higher overall energy intake among those children eating
breakfast (Rampersaud et al., 2005). Potential explanations for this result include lower levels
of physical activity among breakfast skippers (Kapantaisa et al., 2011; Rampersaud et al.,
2005) and higher metabolic rates in breakfast eaters due to more frequent food consumption
(Deshmukh-Taskar et al., 2010). Longitudinal studies have yielded inconsistent results,
possibly reflecting the more diverse range of factors that contribute to food consumption
behaviours as children age (for a review see Affenito, 2007).
Aside from implications for weight status, breakfast consumption has other favourable
nutritional outcomes. Diet quality overall is better among children who eat breakfast relative
to those who do not (Sampson et al., 1995; Utter et al., 2007; Williams 2007), and higher
intakes are achieved of specific positive nutrients such as fibre and calcium (Barton et al.,
2005). Further advantages can be accrued in the form of cognitive or academic performance
(Hoyland et al., 2009). Those children consuming breakfast tend to score better on working
memory tests (Cueto, 2001; Mahoney et al., 2005), and there is some evidence that they are
better behaved in class (Kleinman et al., 2002). Those who regularly consume breakfast in
both childhood and adulthood have been found to have better heart health in later life than
those who do not (Smith et al., 2010)
Given the importance of the breakfast meal, there is growing research interest in
identifying those individuals who are most likely to be at risk of missing breakfast (Keski-
Rahkonen et al., 2003; Rampersaud, 2009). As a result, studies to date have mainly focused
on determining the prevalence and correlates of breakfast skipping (e.g., Pearson et al., 2009).
Estimates of breakfast skipping among children range from 5% to 30%, depending on the
particular country and the age of the children studied (Rampersaud et al., 2005; Tin et al.,
2011). There is a trend for skipping to become more frequent as children enter their teens and
have greater discretion over their food consumption behaviours (Shaw, 1998; Utter et al.,
2007). Skipping has also been found to be more common among children from single parent
families (Croezen et al., 2009; Deshmukh-Taskar et al., 2010; Pearson et al., 2009), those
whose parents do not eat breakfast regularly (Pearson et al., 2009), and those of low SES
(Delva et al., 2006; Deshmukh-Taskar et al., 2010; Utter et al., 2007). These contributing
factors point to the importance of the family environment in determining children’s breakfast
consumption behaviours and highlight the need to view the family as the relevant unit of
analysis.
While prevalence studies are growing in number, relatively little work has examined
children’s motivations for consuming or skipping breakfast and for consuming particular
kinds of breakfast foods. The limited existing work on motivations has typically focused on
adolescents (Kapantaisa et al., 2011; Miech et al., 2006; Niemeier et al., 2006; Thompson-
McCormick et al., 2010; Zullig et al., 2006). Among teenagers, especially girls, skipping
breakfast has been found to be used as a means of weight management (Affenito, 2007;
Kapantaisa et al., 2011; Zullig et al., 2006). Other identified reasons include tiredness upon
waking and a lack of time in the morning for meal preparation and consumption (Affenito,
2007). Given the higher rate of breakfast skipping among adolescents, the focus on this
segment of the population is understandable. However, the earlier childhood years are
important in establishing taste preferences and food consumptions habits (American Dietetic
Association, 2004), making it important to appreciate how breakfast behaviours originate and
consolidate during these years. The greater tendency for skipping in low SES families and the
higher rates of overweight and obesity among members of this group indicate the need to
focus on these families in formative research (Miech et al., 2006). Given the lack of prior
work in this area, such information would be of value to policy makers seeking guidance on
appropriate means of (1) encouraging breakfast consumption in families at higher risk of
breakfast skipping and (2) informing families of the kinds of foods that are most appropriate
for consumption at the breakfast meal.
The present study provides some preliminary insights into the contextual factors relevant
to breakfast consumption behaviours among low SES families in Australia. The findings are
useful in depicting the complex and often difficult circumstances in which low SES parents
attempt to deliver a healthy diet to their children.
Method
Ethics clearance was obtained from a university ethics committee. In accordance with the
approval requirements, all of the study participants were given information documents and
were asked to sign consent forms prior to the commencement of data collection.
A longitudinal, qualitative study was undertaken with low SES parents of overweight
children. The broad aim of the study was to explore the motivators, facilitators, and barriers
relevant to these parents caring for their children’s health. Breakfast was spontaneously raised
numerous times as an important but difficult aspect of parenting and hence became a topic of
particular focus during data analysis.
The study was originally planned as a six-month project involving 50 parents, but
ultimately ran for 12 months with a smaller sample. A social research agency used a random
digit dialling process to identify potential participants with the following characteristics: at
least one child aged five to nine years with a body mass index that placed them in the
overweight or obese category (as per Cole et al., 2000); a gross annual household income of
less than AU$60,000 (the national average household income was $73,000: Australian
Bureau of Statistics, 2008); and no tertiary education qualification. The selection of the five to
nine years age range for the children reflects the importance of this developmental stage for
the onset of overweight and obesity (American Dietetic Association, 2004). Parents provided
their children’s height and weight details to enable calculation of body mass index to
determine eligibility to participate in the study.
In line with recruitment difficulties encountered in previous research with low SES study
participants (Blumenthal et al., 1995; Heinrichs et al., 2005), the research agency experienced
considerable difficulty identifying willing parents who fit the eligibility criteria. This was at
least partially the result of the high level of participation required by the study. Potential
participants were advised that they would be expected to provide fortnightly self-
introspections on topics of their choice relating to child health and attend two individual
interviews and a focus group. The introspections could be submitted by mail, email, weblog,
or telephone recorded message and the individual interviews could be undertaken at any
location preferred by the participant (most chose their homes). The focus groups were held on
a university campus.
Table 1. Participant characteristics
Category Description Quantity

Gender Women 35
Men 2
Family structure Dual-parent families 14
Single-parent families 23
Employment status Working full time 6
Working part time 7
Parenting full time 24
Child gender ‡ Female 25
Male 14
Child weight status ‡ Overweight 20
Obese 19
No. of children in family 1 child 5
2 children 17
3 children 8
4+ children 7
‡Total adds to more than 37 because some parents had more than one overweight or obese child in the
specified age range.
Reflecting the level of commitment required by the research, potential participants were
advised that they would be paid $75 per month over the course of the study, with proportional
payments made to accommodate any reductions in participation relative to expectations. The
average monthly payment made to participants was $71. Ultimately, just 37 parents
commenced the study, almost all of whom were mothers. Table 1 provides the sample profile.
Of note is the relatively high proportion of single parents, which reflects the substantially
higher rates of single-parent families among low SES households (Australian Bureau of
Statistics, 2007). Given this smaller than anticipated starting sample and the ongoing
commitment of the participants once they had become involved in the study, the decision was
made at the six-month point to extend the study to a full year. Twenty-seven of the
participants were still involved at this stage, 22 of whom agreed to continue for the full 12
months. All data collection episodes were audio recorded or captured online, and
subsequently transcribed. The result was 588,734 words of data that were imported into
NVivo 9 for coding and analysis. A thematic approach was used to interpret the data and
produce findings of relevance to public policy makers attempting to prevent child obesity.
Findings
Throughout data collection and analysis, it became clear that breakfast is a particularly
contentious food consumption occasion for most of the families participating in the study.
Almost all of the parents noted the importance of breakfast and expressed a desire for their
children to consume a healthy meal in the morning to ensure they could function properly
during the day:
The children have to have good breakfast in the morning – drink milk, another protein
food, such as an egg, cheese, or meat, a slice of white bread or wholemeal toast or a bowl of
cereal - so they can have energy and concentration at school. (Adeline, single, four children,
handwritten introspection)
However, for many of the study participants it was a challenge to make this aim of daily,
healthy breakfasts a reality. As noted by one mother, “Breakfast is a really hard meal to get
them to have” (Kathryn, single, two children, phone bank message). Breakfast was often
spontaneously raised by the parents as a particularly problematic aspect of managing their
children’s diets because of the numerous factors that in combination make it a pressured food
consumption occasion. While a minority described breakfast in their household as being
‘under control’, many others nominated numerous elements of breakfast organisation,
delivery, and consumption as being a source of concern and conflict. These elements are
categorised into themes as outlined below.
Kids Rule, OK?
In line with their views about the importance of breakfast, the majority of the participants
reported going to some lengths to ensure their children ate breakfast prior to leaving home in
the morning. However, it was clear than in many instances the children had the upper hand in
terms of the type of food consumed. Constrained by their desire to ensure their children did
not skip breakfast altogether, many parents reported that their children ate sub-optimal
breakfast foods because their children’s taste preferences were permitted to determine the
food items that were purchased and consumed:
At least if they’ve eaten something, you know what I mean? I know it’s high sugar, I
know all the wrongs and all that, but it’s just, if they’re going to refuse and not eat anything,
it’s like, well, I’d just prefer them to have something in their stomach, anything. Yeah, I mean
something else will keep them satisfied longer, of course, but at least, I sort of think, at least it
will keep them full for half an hour, you know what I mean? (Natasha, living with partner,
two children, interview)
A fear of their children refusing to eat at all, combined with a desire to avoid early
morning conflict in the home, appeared to often result in some children being able to
effectively manipulate their parents into providing foods, despite concern among the parents
that the foods were nutritionally inadequate. Natasha went on to explain further as follows:
I’m a mean mum if I don’t supply this, the high sugar cereals. I tried them not having
anything, and they just wouldn’t have anything. So it’s like, well, what do you do? They just
refuse to eat it, so you know what I mean? (Natasha, living with partner, two children,
interview)
For some, this acquiescence in relation to the types of foods consumed constituted a
reward for the children complying with the logistics of getting up and ready on time.
Especially for working parents, the breakfast plan that worked best was the one that enabled
children to make the food selection decisions:
I believe it is hard to get kids to eat breakfast. And I do give them whatever they want.
Well, see, in the mornings my girls come into work early with me in the morning at 8 o’clock.
They come through at the back of the workshop and they pick out a milkshake, or Up & Go.
Tabitha always picks the Up & Go and Renee gets the iced coffee, and they walk to school
with it. That’s their little reward to come to work with me and get up, and the boss lets them
come through and everything. They’ve got like a five minute walk to school, so they’re
having a drink, walking, and so I do give them whatever they want for breakfast with the
cereals… Yep, I just give them what they want to eat for breakfast. (Veronica, single, four
children, interview)
Children’s tiredness and their lack of hunger until they had been awake for a period of
time were often reported to make children difficult to feed in the morning. While most
participants responded to this situation by either allowing their children to eat unhealthy
breakfast foods or skip breakfast altogether, the foster mother quoted below had learned over
the years to ensure that the children in her care were woken up in time to develop an appetite
for breakfast.
Everyone has to have breakfast. The boys never would eat breakfast when they came to
my care, they refused to eat breakfast. They weren’t hungry when they got out of bed. I learnt
to wake them up earlier. (Claudia, single, one child plus foster children, interview)
For just a few, the power of the children in the household resulted in the parents being
unable to influence their breakfast consumption at all, resulting in breakfast being skipped at
the child’s whim:
With Jane, she very rarely has breakfast. I always offer it and encourage it, but if she
doesn’t want it, she won’t have it. (Tara, single, three children, focus group)
This refusal to consume breakfast by the child can have negative outcomes for both the
child and the family, as described in the quote below. Despite these undesirable and highly
unpleasant consequences, which would presumably act as a strong motivator, these parents
were not able to conceptualise and implement strategies to overcome their children’s
reluctance to have breakfast:
There are, you know, quite regularly days when he doesn’t have breakfast, doesn’t have
lunch. He comes home and is absolutely ravenous, obviously, and yells and screams and
fights. (Emily, single, three children, interview)
A strategy used by some participants to prevent conflict with their children over the types
of breakfast foods that were available in the home was to compromise by purchasing foods
that were attractive to their children while also having attributes of importance to the parent.
As explained in the following quote, there are trade-offs that can be made that result in both
the parent and the child being satisfied with the food choice:
It’s the good of the devil. You’ve got all these devils and I’m trying to choose the best
devil, vitamins sprinkled on top. It’s like with the white bread. If I’m going to have white
bread, I’ll try to get something that’s got high fibre in it or low GI. So even though it’s bad,
it’s still the better of the bad. (Natasha, living with partner, two children, interview)
While many of the participants appeared to experience a lack of control over their
children’s food consumption in the mornings, this outcome was not uniform within
households. Participants often drew comparisons between their children’s diets to illustrate
their variable ability to ensure their children consumed a healthy breakfast. The implication
seemed to be that the problem was the specific child rather than their parenting skills. While
this may to some extent be the result of different breakfast consumption behaviours that
emerge as children grow older (Niemeier et al., 2006; Utter et al., 2007), there were sufficient
variations in the age and birth order of the problematic child to indicate that this is an
incomplete explanation. Instead, it appeared that different children within families can bring
different issues to the breakfast table:
My middle child (age 7) has breakfast every morning, cereal every morning. My oldest
child (age 9) is difficult – we’re lucky if we can get an apple into her at breakfast time.
(Danielle, married, three children, interview)
I try not to worry about her because she says she’s not hungry, and she went off this
morning without having breakfast. But the other two, Amy (age 8) will always have her Weet-
Bix or cereal and Timothy (age 10) will have toast, but Lynda (age 13) won’t. (Isabela,
married, six children, interview)
James (age 9) always has a very good appetite and he always has his Weet-Bix and then
his piece of toast. Anna (age 6) will sometimes eat it, and other times say, ‘I’m not hungry’.
(Melina, married, two children, interview)
Nutrition Confusion
Confounding the control issues referred to above was some confusion relating to the
nutritional profile of various breakfast foods. Most participants nominated Weet-Bix and oats
(porridge) as being superior breakfast foods:
Weet-Bix, yes, healthy, healthy. (Tara, single, three children, focus group)
We hardly buy those Coco Pops and stuff like that. We get Cornflakes and porridge and
Weet-Bix. (Melinda, single, four children, paired interview)
Lately I’ve been buying Nutri-Grain and Honey Puffs and I think they get hungry faster
than if they have just Weet-Bix or porridge. Porridge lasts longer. (Naomi, married, three
Breakfast cereals that are high in sugar were generally recognised as being poor choices.
Commonly mentioned examples were those that are heavily promoted to children, such as
Coco Pops and Froot Loops:
I know that all the cereals are bad. A lot of people get tricked with the cereals, like I’ve
got Coco Pops and stuff, but I only let them have that on the weekends. (Claire, married, two
These assessments coincide with those of a major nutritional review of Australian

breakfast cereals by CHOICE (2010), the nation’s primary consumer organisation. However,
with almost 200 cereals on the market, the participants found themselves struggling to
evaluate the relative and absolute healthiness of many other product offerings. None of the
participants mentioned referring to the nutrient information panel on cereal packets, instead
relying on marketing information located on the front of the pack and contained in
advertisements and word-of-mouth communications received from family and friends:
I’ve got issues with Cheerios though. I think they’re good - it says good stuff on the
package. (Claudia, single, one child plus foster children, interview)
My kids love Nutri-Grain, and I always thought Nutri-Grain was good. Then not long ago
I got told, ‘No, it’s really bad. It’s like Coco Pops.’ So I won’t let my kids eat Coco Pops or
Froot Loops…I think it was my brother who said, ‘Nah’, and he was watching something on
the TV and he was like, ‘Nutri-Grain is really bad. You might as well give them Froot Loops.’
Yeah, he said, ‘Nah, it’s really bad for them.’ And then my mum was like, ‘Yeah it’s really
high in sugar.’ I didn’t know that. (Marion, single, two children, interview)
In their evaluations, participants focused mainly on added sugars, and to a lesser extent
fibre. There did not seem to be an appreciation that breakfast products may also be high in
salt and fat and that a range of other important nutrients are contained within breakfast foods
(e.g., folate, iron, zinc, magnesium, potassium, and vitamins A, B6, B-12, and C: Deshmukh-
Taskar et al., 2010).
I’m also aware of how bad our cereals are, and the sugar that’s in it. Elise is going to the
dentist and they have to do a lot of work on her teeth, and I think it’s just those little incidental
things that you don’t think are bad, like your cereal. And because I have Special K and the ad
says, ‘It will keep you looking good if you have special K’, and um, and I thought I was doing
really good. But when I went to the dentist and that was one on their list to say that it was high
in sugar, but when you eat it, I can’t taste sugar in it, so to me it doesn’t taste like there’s sugar
in it. So they have Cheerios, which I don’t think are fantastic either way. (Marilyn, married,
three children, interview)
I like Weet-Bix. To me it’s a good solid, fibre to start off the day with. (Rachel, married,
three children, interview)
There appeared to be a general belief among participants that there exists a nutritional
hierarchy among breakfast foods that has a cooked breakfast at the top, followed by healthy
cereals, then less-healthy cereals, then bread. Fruit was also considered to be appropriate
breakfast food, although inadequate on its own to constitute a complete breakfast.
Ezra is right into having an omelette for breakfast, a one-egg omelette. I think that’s quite
healthy, so I’m thinking it’s better than bread. (Natasha, living with partner, two children,
interview)
Depending on how I go with my shopping, they’re allowed to pick out a special cereal,
which usually lasts two days because they will eat it a lot. Like things like Coco Pops. But
now I’ve got a bit relaxed with the shopping and they will eat that over eating Weet-Bix and
it’s just not sustaining them. They’re still hungry, but they have toast in the morning as well,
but they’re still hungry before recess. (Laura, married, four children, interview)
The assumption that a cooked breakfast is the ideal way to provide the energy needed by
children for their daily activities runs counter to research that has found the consumption of
such foods to be more likely to be associated with higher BMI and lower intake of positive
nutrients compared to children consuming cereals (Barton et al., 2005; Deshmukh-Taskar et
al., 2010; Preziosi et al., 1999). However, the belief among some participants that high-sugar
cereals constitute a better alternative to bread products may also be problematic. At 37%
sugar, it is unlikely that Coco Pops was a superior choice to bread in the context described in
the quote below:
He’d generally always just have his two slices of toast in the morning, and by that stage
it’s just like, ‘Come on mate you’ve got to have something else.’ I’m thinking, ‘I don’t care if
it’s a bowl of Coco Pops you know, you can’t have your two slices of bread in the morning
and then have a sandwich, you know, like your two slices of bread for your sandwich.’ And
then, depending on what we would have for dinner, he’d have a slice of bread to dip in. And
it’s like, ‘That’s too much bread, you’ve got to have cereal.’ So yeah, now he pretty much just
gets into his Coco Pops and his Rice Bubbles. (Brenda, single, two children, interview)
Related to the hierarchy concept was the perception that more breakfast food is better
than less. The overall healthy connotation of the breakfast meal appeared to translate into a
desire among parents to get as much food into their children as possible at this meal. This was
most notable among those parents who prided themselves on having children who would eat
healthy breakfast foods:
I pour a bowl for cereal for her the same size as mine, you know, because I just don’t
want her to go hungry. But it is the wholegrainy sort of cereals, like porridge and that. (Carey,
married, two children, interview)
Kaden, a little while ago at 18 months, he’d be having five Weet-Bix to himself, and he’d
want more. We were just like, ‘Where does it all go?’ (Laura, married, four children,
interview)
Compliance Issues
Some parents acknowledged that they often skipped breakfast themselves, and that their
children were aware of their failure to live by the rules they attempted to apply to the younger
members of the family. These participants felt that their own suboptimal breakfast behaviours
made it difficult for them to legitimately require their children to consume a healthy
breakfast:
I always tell him, ‘Mate you have to have breakfast before you go to school. You need to
be able to concentrate, it will help you concentrate. You have to have breakfast.’ But yeah, I
feel like a bit of a fool because I don’t eat breakfast, I don’t eat lunch. (Brenda, single, two
They have got all my bad habits I think. They won’t eat breakfast. (Yvette, single, three
The situation can become considerably more complicated where parents are estranged or
in a fractious relationship, and hence may not communicate a unified message about the kinds
of foods that are most appropriate for breakfast. In the quote below, Claudia explains below
that when children spend time with the other parent, it may not be possible to maintain a
healthy breakfast routine:
The mum needs the dad to come and back it up. They (fathers) just think it’s okay to give
them what they want to shut them up. That’s parenting the wrong way, but that’s their
prerogative because they’re dad. (Claudia, single, one child plus foster children, interview)
Discussion
Previous research examining children’s breakfast consumption behaviours has mainly
focused on the act of breakfast skipping and its correlates (Barton et al., 2005; Cheng et al.,
2008; Deshmukh-Taskar et al., 2010; Delva et al., 2006; Dubois et al., 2006; Sampson et al.,
1995; Shaw 1998; Tin et al., 2011; Vanelli et al., 2005). The few studies that have identified
the range of characteristics and behaviours associated with breakfast skipping have typically
surveyed adolescents (e.g., Kapantaisa et al., 2011; Miech et al., 2006; Niemeier et al., 2006;
Thompson-McCormick et al., 2010). There is thus a lack of research relating to younger
children and the factors affecting their breakfast consumption behaviours.
The present study accessed the lived experiences of low SES parents of overweight
children to explore the factors that influence their children’s breakfast-related behaviours. As
noted in the literature, it is important to focus on low SES children in this context because of
their higher levels of obesity and their less favourable breakfast consumption habits (Miech et
al., 2006). The selection of families with younger children reflects the importance of this
developmental stage for food-related preferences and habits (American Dietetic Association,
2004).
The main themes to emerge from the research were (1) parents’ perceived lack of control
over their children’s consumption of unhealthy breakfast foods, (2) inadequate knowledge
relating to optimal breakfast foods, and (3) the potential for more consistent parental
modelling of breakfast consumption. Given the few previous studies that have explored this
issue from the perspective of parents of young children, there is little prior research with
which to compare these findings. It appears that this is among the first studies to provide a
detailed qualitative analysis of how lower SES parents attempt to cope with the various
factors that can impede their efforts to ensure their children consume a healthy breakfast each
day.
The finding that some parents perceive they must make a trade-off between their children
eating sub-optimal breakfast foods and not having breakfast at all suggests that they are not
fully appreciating their role of food provider. While children are still young, parents largely
have control over the food options available (Birch and Fisher, 1998). Food preferences are
determined early in life (American Dietetic Association, 2004), and it often takes repeated
samples of foods to foster a liking for them (Birch et al., 1987; Birch and Marlin, 1982). As
genetic predisposition makes foods high in sugar, fat, and salt highly palatable, it can take
effort to cultivate preferences for healthy foods in the presence of these alternatives (Blass,
2003). This phenomenon has resulted in unhealthy foods being labelled ‘competitive foods’
(Bhatia et al., 2011), as by their very presence they can discourage the consumption of
healthy foods. The tendency for parents in this study to frequently purchase high sugar cereals
is likely to create an environment in which their children reject healthy options because of the
ready availability of ‘tastier’ alternatives. Interventions may be needed that focus on
encouraging parents to persevere in developing a preference for healthy breakfast foods in
their children from a very early age and to ensure unhealthy options are generally unavailable
in the home.
Related to this issue of product alternatives is the opportunity to provide parents with
clearer information about the nutritional quality of the large number of breakfast cereals on
the market. The tendency for the participants to rely on word-of-mouth and marketing
communications rather than the detailed, accurate information contained in the nutrition
information panel located on the back of food packages highlights the need for nutrition
information to be provided in a more user-friendly manner. Numerous studies have
demonstrated the efficacy of easy-to-understand front-of-pack nutrition labels in providing
consumers with information that they can use to select between competing product offerings
(for a review see Grunert et al., 2012). ‘Traffic light’ front-of-pack food labels that indicate
whether levels of nutrients such as fat, sugar, and salt are low, medium, or high have been
found to be especially effective in conveying nutrition information to low SES consumers
who are likely to lack literacy skills (Borgmeier and Westenhoefer, 2009; Gorton et al., 2008;
Kelly et al., 2009; Louie et al., 2008). The findings of the present study suggest that efforts to
implement a front-of-pack labelling system that is readily comprehensible to low SES parents
could assist them in their efforts to navigate the cereal aisle to select products that are
appropriate for daily consumption by their children.
Finally, the findings highlight the need to address food consumption issues at the family
level to ensure that parents are both facilitating a healthy diet for their children and modelling
the consumption of this diet. The importance of parental modelling in preventing and treating
child obesity is depicted in Golan’s (2006) model of family-based health. This model
emphasises the need for parents to have appropriate knowledge and skills to enable them to
influence their children’s weight status via two pathways: (1) directly through communication
about healthy eating and the setting and enforcement of appropriate household rules and (2)
indirectly by modelling the desired behaviours. The findings from the present study indicate
that low SES parents can struggle to establish rules relating to appropriate breakfast
behaviours and to model compliance with these rules. This suggests that interventions may
need to focus on providing parents with the knowledge and skills required to achieve these
outcomes. As noted by Niemeier et al. (2006), the specific nature of breakfast consumption
behaviours can facilitate the development of targeted interventions that aim to modify the
factors influencing these behaviours.
The present study is limited by the small sample size and the confinement to one state in
Australia. However, the findings provide an important starting point for future research
through the engagement of more representative samples and broader geographical coverage.
The longitudinal nature of the study provides some assurance of the robustness of the findings
and their utility for informing future work in this area.
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Chapter V
Early Vitamin D Supplementation,

Immune Modulation and Allergy
Gian Vincenzo Zuccotti and Valeria Manfredini

Department of Pediatrics, Luigi Sacco Hospital, University of Milan, Milan, Italy
Abstract
A daily Vitamin D (VitD) intake of at least 400 IU/day is recommended nowadays
by most updated guidelines during the first year of life. However, it is not known whether
such an intake is enough to provide all the health benefits associated with VitD and a
consensus is still missing stating the serum vitD levels appropriate for global health and
the cutoffs for deficiency in younger individuals.
Potent immune-modulating effects of VitD have been reported in vitro and, in
particular, its potential ability to influence both innate and adaptive immunity, reducing
the inflammatory response associated with Th1 and Th17 cells and skewing the T cell
balance towards a Th2-phenotype.
VitD immune-modulation activities could thus play a role in controlling infections
and reducing inflammatory responses toward viral pathogens in both children and adults.
However, the evidence in relation to vitD and allergic diseases is controversial.
Most evidence report a protective effect of vitD against allergy. Some studies,
however, suggest that VitD supplementation can be a risk factor for asthma and atopic
disorders, assuming that VitD could induce sensitization against allergens during infancy.
In this chapter, published data on the relationship between vitamin D and asthma and
allergy will be discussed, emphasizing the need for controlled, prospective studies on
vitamin D supplementation to clarify whether it has a role in the prevention of and
treatment for asthma and allergic conditions.
Introduction
In younger individuals, Vitamin D (VitD, cholecalciferol) deficiency and insufficiency
lack a precise definition. The recent guidelines issued by the American Academy of
108 Gian Vincenzo Zuccotti and Valeria Manfredini
Pediatrics, the Canadian Pediatric Association and the Institute of Medicine recommend,
however, a daily intake of VitD of 400 IU/day during the first year of life to target a serum
value for 25(OH)D of at least 50 nmol/L (20 ng/mL)[1-3]. This value is supposed, in facts, to
meet the needs of nearly all children and is lower than that recommended by some experts
referring to adult population [4], for which there is no consensus either [5].
Owing to the recent evidence regarding its immune-modulatory properties, it has been
postulated that VitD can be involved in the pathogenesis of several diseases associated with
pathological Th1 phenotypes (multiple sclerosis, juvenile rheumatoid arthritis and type 1
diabetes) or Th2 responses (lupus erythematosus sistemicus) [6-9]. Moreover, VitD immune-
modulation activities may also act in controlling infections and reducing inflammatory
answers toward viral pathogens in both children and adults [10]. The evidence related to VitD
and allergic diseases is, however, controversial. Even if most studies report a protective role,
some suggest that VitD supplementation can be a risk factor for asthma and atopic disorders,
suggesting a VitD-triggered sensitization against allergens during infancy [11-16]. The
industrial revolution has dramatically reduced the daily sun exposure, increasingly moving
the everyday life from outdoor to indoor and promoting the growing prevalence of obesity in
both adults and children [17]. Altogether, these lifestyle changes have favoured the reduction
of VitD plasma levels and led to the growing prevalence of VitD insufficiency and deficiency
along with its consequences on bone health [18, 19]. Especially in Western countries, where
VitD insufficiency is a surprisingly common finding, the concurrent rising pandemic
incidence of allergic diseases has lead some investigators to consider VitD playing a major
role in the prevention and treatment of several atopic disorders among which are asthma and
skin eczema [20].
Since 1999, conversely, Wjst and Dold have supported the idea that the observed increase
in asthma and allergy was the consequence of a widespread VitD supplementation used for
rickets prophylaxis, appealing to the immune modulating properties of 25-OH-D possibly
driving the Th2 responses and favouring the development of allergic phenotypes [11, 12].
Following such theory, other authors have attributed the initial sensitisation against allergens
during the newborn period to undetermined and undefined immunological effects of vitamin
D supplements used for rickets prevention [14, 15, 21].
Undoubtedly, Vitamin D plays a complicated role and interacts with the genetic
predisposition of each single individual, the modification of the lifestyle habits following the
growth of industrialisation and the increasing exposure to pollution in the environment,
possibly bridging immune function, inflammatory/infectious and allergic diseases.
Vitamin Metabolism and Immune Modulation

VitD is a secosteroid that shares a close structural and functional resemblance to steroids
and acts on target cells with a similarly hormone-like mechanism, binding a specific nuclear
Vitamin D receptor (VDR). The ligand receptor complex derived from this interaction acts on
specific DNA sequences called the “vitamin D responsive elements” and allowing the
transcription of several molecules, among which are proteins involved in the calcium-
phosphate metabolism [22].
Early Vitamin D Supplementation, Immune Modulation and Allergy 109
In humans, VitD is mainly produced from cholesterol in the skin after ultraviolet B
exposure and is called cholecalciferol. A lesser amount of the vitamin is directly ingested
with vegetables and some fungal sources and is known as ergocalciferol (Vitamin D2). To
become active, VitD undergoes a two-step hydroxylation process. Two enzymes are involved,
the first located in liver cells and leading to the production of the mono-hydroxilated form,
the 25-OH-D, and the second, the 1-α-hydroxylase enzyme, found in kidney proximal renal
tubule cells and allowing the conversion of the 25-OH-D to its final bioactive form, the 1,
25(OH)2D. In humans, the 25-OH-D accounts for the major amount of the circulating element
[23]. In the text, however, we will refer alternatively to VitD as cholecalciferol, 25-OH-D or
1, 25(OH)2D.
For many years, the role of VitD in immune modulation has been postulated observing
that infants with rickets underwent respiratory infections more frequently than infants without
rickets [24]. Nowadays, this theory has found support in the evidence that the 1-α-
hydroxylase enzyme, the key-step of the activation cascade, is present not only in the renal
tissue but also in cells of the immune system and that the VDR is similarly found in T cells, B
cells, NK cells, and monocytes. Moreover, at least four VitD receptors genes exist as heritable
traits, thus possibly making VitD sensitivity a genetically determined individual peculiarity
[25].
The activation of the VDR has so called non-classical effects including the modulation of
growth, differentiation status and functions of various immune targets, especially playing a
role in T and B cell regulation. In particular, over 102 genes have been identified in CD4+ T
cells being targeted by the VitD [26].
Cholecalciferol-related anti-inflammatory and immune-regulatory properties have been
largely analyzed mainly by studies in vitro.
Starting from innate immunity, research has shown that VitD inhibits the expression of
the Toll-like receptors (TLRs) on monocytes and reduces the TLRs-mediated inflammatory
cascade [27]. In addition, VitD acts hosting the differentiation of macrophages into Dendritic
Cells (DCs), promoted by the exposure to antigens part of the microbial surface (e.g. the
lipopolysaccharides). This process not only leads to the inhibition of DCs maturation,
activation and survival but also determines a reduced stimulatory activity on T cells and a
decrease of their inflammatory mediators release [28, 29]. Among all cytokines and
chemokines produced by the DCs and inhibited by the interaction with VitD are the IL-12 and
IL-23, which are major drivers of the Th1 and Th17 differentiation [30]. Not surprisingly, the
pro-inflammatory response associated with Th17 cell phenotype has resulted to be similarly
inhibited in both mice and humans supplemented with cholecalciferol [31].
In addition, animal models have shown that VitD enhances the T cell proliferation after
antigen exposure and, in particular, the Th2 lymphocyte cytokines (IL-4 and IL-13), possibly
skewing the T cell balance towards a Th2-phenotype [32]. Moreover, murine studies have
shown that the active vitamin D hormone, the 1, 25(OH)2D, is able to promote an immune
response with interleukin IL4- and IL13-driven IgE production in mice genetically non-biased
for TH2-type responses [33]. However, information related to this issue are still controversial
[34, 35]. Further animal models, in particular, have shown that VitD supplementation is also
accompanied by the increase of an anti-inflammatory answer and enhanced regulatory
response from driven T cells. This is supported by data showing that cholecalciferol does not
solely sustain and modulate the T helper function, but also regulates the T regulatory cell
(Treg) activity [36]. To further sustain of this issue, it was shown that VitD stimulates the
DCs to release not only IL-10, which has broad-spectrum anti-inflammatory activities, but
also the chemokine MIP-3α, which is involved in the recruitment of CCR4-expressing Treg
[37]. Besides DCs, also the antigen-presenting and T-cell stimulatory capacities of
monocytes/ macrophages are greatly inhibited by the 1, 25(OH)2D. This is demonstrated by
the inhibitory effect of the 1, 25(OH)2D on the surface expression of MHCII and co-
stimulatory molecules, such as CD40, CD80, and CD86 on antigen presenting cells [38, 39].
Finally, physiologically relevant concentrations of 1, 25(OH)2D have proven to enhance
autophagy in human macrophages, possibly playing a key role also in the defence against
opportunistic infections [40].
In summary, the 1, 25(OH)2D indirectly shifts the CD4+ T-cell polarization from an
inflammatory Th1 and Th17 to a Th2 and regulatory T-cell phenotype. How the Th2 or the
Treg dominance is prevailing during supplementation with cholecalciferol and whether VitD
induces or decreases, respectively, the in vivo antigen sensitisation is still an open question.
Maternal Vitamin D
Supplementation and Allergy
Most recent evidence is sustaining the hypothesis that VitD exposure might influence the
predisposition to allergies already in utero and soon after birth, during the first developmental
phases of the immune system [41].
During pregnancy, the foetus is exposed to vitamin D that crosses the placenta through
the cord blood and is entirely dependent on its mother for supply. Thus, reduced
concentrations of 25-OH-D and poor maternal intakes during pregnancy may reflect in the
infant at birth and decrease VitD stores during the first months of life [42]. An inverse
association between maternal 25-OH-D intakes during pregnancy and the risk of childhood
wheezing was demonstrated in a well designed longitudinal prospective study performed in
Japanese population by Miyake and colleagues. Authors were the first to find that maternal
intake of total dairy products, milk, especially full-fat milk, cheese and calcium during
pregnancy was independently related to a decreased risk of wheeze in children aged 16 to 24
months. Moreover, they found that children whose mothers had consumed daily 4.309 mcg (≈
100 IU) or more of vitamin D during pregnancy had a significantly reduced risk of both
wheeze and eczema [43]. Later on, a retrospective analysis by Algert and colleagues,
including a large birth cohort of 240, 511 singleton infants born during 2001-2003, found a
significantly increased risk of asthma in children conceived and born in autumn and winter
seasons. To explain such seasonal variations, authors assumed that the prevalence of the
disease was inversely related to the lower levels of VitD, resulting from a reduced sun
exposure during the first trimester of pregnancy [44].
When cord blood 25-OH-D levels were used to assess the association between VitD
status at birth and allergic outcomes, contrasting findings were observed. Rothers and
colleagues found that both low (<50 nmol/L) and high (≥ 100 nmol/L) levels of cord VitD
were associated with increased total IgE and detectable inhalant allergen-specific IgE up to 5
years of age. Notably, however, the 25-OH-D levels were not significantly related to allergic
symptoms such as rhinitis or asthma [45]. Camargo and colleagues similarly found no
association between the 25-OH-D cord-blood levels and asthma incidence. However, an
inverse relation emerged between recorded vitamin D cord-blood concentrations and the risk
of respiratory infection and childhood wheezing.
Direct measures of maternal levels of 25-OH-D were taken by Gale and colleagues [46].
The authors showed that 25-OH-D concentrations greater than 75 nmol/L (30ng/mL) during
late pregnancy significantly related to a higher risk of atopic eczema at 9 months, and asthma
at 9 years in the offsprings. Maternal circulating 25-OH-D concentrations were similarly
measured during pregnancy in a population-based study including a large birth cohort of 1724
newborns [47]. One year after delivery, data were collected regarding the incidence of a
physician-confirmed history of lower respiratory tract infections or a history of wheezing
during the first 12 months of life in their children. The same questions about wheezing were
annually repeated thereafter and asthma was defined as parental reporting of doctor’s
diagnosis of asthma or receiving treatment at the age of 4 to 6 years or wheezing since the age
of 4 years. Results showed that higher maternal circulating cholecalciferol levels were
independently associated with a decline in the risk of respiratory tract infections but the same
relation was not confirmed for wheezing and asthma. Finally, maternal circulating 25-OH-D
levels were more strongly associated with the risk of respiratory tract infection in the
offspring born during autumn and winter months, when maternal Vitamin D mean seasonal
levels were presumptively lower.
Even though such reports suggest that low VitD levels may play a part in the
etiopathogenesis of asthma and allergy, it must be noticed that none of the available studies
measured VitD directly in newborns, simply looking at maternal intake, season of birth, cord
or maternal blood concentrations of cholecalciferol as a proxy for its levels of exposure in the
newborns, mostly neglecting the contribution of UV radiation to physiological status. It must
be also considered that confounding factors should be taken into account when different
populations are studied. Consumption of fish, for example, provides a great amount of n-3
fatty acids but is also a major source of VitD in some population, for example the Japanese
[48]. In American women, instead, Vitamin D is mainly ingested through fortified milk that
lacks in polyunsaturated fatty acids. Such differences could explain why, in the above
mentioned study from Miyake and colleagues, the inverse relation between maternal VitD
supplementation during pregnancy and wheeze occurrence in Japanese children was found
only after data were adjusted for maternal docosahexaenoic and α-linolenic fat acid intake
assumed through fish consumption and contemporarily increasing the VitD intake. Finally, it
must be noticed that in most studies a weak relationship was found to exist between VitD
levels and asthma in childhood. Whereas, the inverse association found between VitD status
and wheezing occurrence was stronger and might be attributed to the immune-modulatory,
anti infectious and anti inflammatory properties related to the vitamin and better described in
the next paragraph.
Vitamin D and Asthma

Examining the outcome of an early VitD supplementation on the course of asthma among
other allergic diseases in children still produces controversial results. In a birth cohort study
from Finland, subjects regularly supplemented during the first year of life with a VitD dose of
200 IU/day, that is lower than that suggested nowadays, have shown to develop a significant
higher risk of asthma, atopy, and allergic rhinitis during adulthood than unsupplemented
controls [15]. In the same year, another study analysed data from more than 8000 patients
provided by the National Centre for Health Statistics (USA) and similarly found that early
VitD supplementation was associated with an increased risk of asthma in black children and
food allergies in exclusively formula-fed children [14].
Notably, none of these studies provided VitD concentrations obtained from children’s
blood samples. In older children, studies in vivo using VitD as a biomarker mainly attribute to
cholecalciferol a protective role and find an inverse relation between VitD plasma
concentrations and the incidence of asthma and allergy symptoms, confirming similar reports
from the adult population [13].
Brehm and colleagues were the first to analyse the relationship between measured 25-
OH-D levels and markers of asthma severity in children selected during a family-based cross-
sectional genetic study of asthma in Costa Rica [49]. The authors found that lower
cholecalciferol levels, less than 75 nmol/L (30 ng/mL), were more frequent in children with
asthma. In these patients, minor VitD concentrations were not only associated with increased
asthma severity, but also with total IgE and eosinophil count. The association between
vitamin D and serum IgE levels was similarly investigated in a group of asthmatic children
and adults compared with healthy controls (HC). Remarkably, although prevalence of low
VitD levels, less than 20 ng/mL, was similar in both patients and HC (47.6% versus 56.8%),
in paediatric asthma group, VitD measures were inversely related to IgE serum concentration
and the daily inhaled corticosteroid dose [50].
The role of 25-OH-D has been also assessed in prospective analysis. Hollams and
colleagues, for example, described the results obtained from 989 six-year old and 1,380
fourteen-year old subjects from an unselected community birth-cohort [51]. When VitD levels
were assessed as a risk modifier for respiratory and allergic outcomes, authors confirmed that
VitD concentrations at age 6 and 14 years were predictive of allergy and asthma outcomes at
both ages. More importantly, VitD levels at age 6 resulted predictive of atopy and asthma-
associated phenotypes at age 14 years in males.
The reduced incidence of asthma exacerbation and gravity observed in vivo may find
explanation by virtue of 25-OH-D normal plasma concentrations favouring a better control of
infections altogether with the reduction of the inflammatory responses toward pathogens.
Through its influence on innate immunity, in fact, it has been demonstrated that VitD favours
the expression of the human cathelicidin antimicrobial peptide (CAMP), enhancing
monocytes/macrophages’ activity also against the mycobacteria [52]. Beside CAMP, it was
also shown in vitro that 1, 25(OH)2D targets the gene of the defensin β2 in a variety of cell
types including myeloid cells, keratinocytes, neutrophils and bronchial epithelial cells [53].
This is particularly relevant in providing support to the host defence against respiratory tract
pathogens and reducing the impact of asthma exacerbations in affected patients. Moreover, it
has been proved that 1, 25(OH)2D modulatory properties on the regulatory T cell function and
interleukin-10 production might also enhance the therapeutic response to glucocorticoids in
steroid-resistant asthma [54].
Despite data regarding VitD status and its effect on asthma pathophysiology are still
lacking, studies in both animals and humans have also been investigating a possible
relationship between serum VitD concentrations and lung structure. Data on mice have
shown, in fact, that VitD deficiency is related to deficits in lung function, primarily explained
by differences in lung volume [55]. Further data in animal models have suggested that 1,
25(OH)2D plays as a local paracrine and autocrine effector of fetal lung maturation and
affects fibroblast apoptosis. Moreover, both 1, 25(OH)2D and its 3-epimer have been proven
to act on interstitial lung lipofibroblasts (LF) and alveolar type II (ATII) cell differentiation,
at once stimulating LF and ATII cell proliferation thorough the inhibition of their apoptosis
[56]. Studies in vivo from the adult population have similarly confirmed the role of VitD in
maintaining and supporting an adequate lung development [57]. In children, Gupta and
colleagues have studied VitD levels and different lung function test parameters in a cohort of
86 patients with therapy resistant or moderate asthma, compared with healthy controls [58]. A
positive relationship was found between FEV1, FVC and vitamin D concentrations in all
subjects. VitD levels were also inversely related with exacerbations and inhaled steroid in
both moderate and severe asthma patients. Not surprisingly, an inverse relation was recorded
between airway smooth muscle mass obtained through fiberoptic bronchoscopy and the
plasma levels of the vitamin.
Vitamin D and Allergic Skin Diseases

Most of the present data regarding the relation between VitD and food allergy mainly
focus on atopic dermatitis (AD) to indirectly assess the impact of VitD on allergic skin
diseases.
Camargo and colleagues first attempted to investigate the relationship between VitD
supplements during pregnancy and AD among other allergic diseases [59]. Authors described
a decreased risk of recurrent wheeze in children whose maternal VitD intake was higher
during pregnancy. However, they could not prove an inverse relation between VitD
concentrations and AD occurrence. Conversely, further analyses performed shortly after
demonstrated that higher maternal serum levels as so as greater intakes of VitD during
childhood were related to a heightened risk of developing AD, collectively supporting the
hypothesis that increased 25-OH-D concentration might take part in the pathogenesis of
allergy-related skin disease [46].
A recent observational study was performed to assess the severity of atopic disorders in
relation to VitD levels in 37 children aged 8 months to 12 years. In their analyses, authors
described a higher prevalence of severe AD in patients with mean 25-OH-D serum levels
always below 30 ng/mL [60].
In a recent analysis, Goetz and colleagues investigated the possibility of therapeutic
benefits related to the use of VitD to treat idiopathic itch, rash, and urticaria symptoms in 63
patients 3 to 80 years of age [61]. In their results, significantly lower levels of 25-OH-D at
baseline were described in responsive patients as compared to subjects unresponsive to VitD
supplementation, thus supporting the idea that symptoms may resolve or improve through the
correction of a detrimental VitD status. To date, randomised controlled trials investigating the
role of VitD supplementation on allergic eczema in children are missing. In adults,
randomised-controlled studies have been performed in order to test the benefits of a
supplementation with cholecalciferol versus placebo in patients suffering form AD [62, 63].
Collectively, results have shown that VitD supplementation dramatically changes the course
of AD in the treatment group, improving symptoms and reducing atopic dermatitis scores
used to stage the extension of the disease.
Few studies have investigated the potential relationship between VitD and other allergic
skin diseases such as urticaria. Data from the adult population have suggested that
significantly reduced values of VitD levels are found in subjects with chronic urticaria as
compared to controls [64].
Both enzymes required to convert 25-OH-D in its active dyhidroxilated form are found in
keratinocytes of the skin [65]. The VitD produced in-loco acts on the VDR that is expressed
in proliferating cells and, in particular, is present on basal keratinocytes. Recent data from
studies in vitro have shown that VitD attenuates and timely resolves the inflammatory skin
responses induced by external injuries [66]. In mice models, the activation of the VDR in the
skin has also been related to the improvement of the allergen-triggered eczema [67]. Data are
missing to confirm the same in humans. It can’t be excluded, however, that VitD may favour
the reduction of symptoms in atopic eczema through modulation of the antigen oral tolerance.
To support such hypothesis, it has been assumed that cholecalciferol could accomplish its
immune function in the enhancement of the mucosal defence and thorough modulation of
lymphocytes’ function in the local gut microenvironment, thus reducing infective episodes of
the gastrointestinal tract. These properties would altogether maintain an healthy microbial
ecology and reduce the creation of possible breaches of barrier and violation of other defences
that might synergistically promote abnormal allergic responses to food antigens, leading to
food allergy in predisposed subjects [68].
A potential explanation to the conflicting connection between VitD and allergic skin
diseases might be found in the nonlinear association between 25-OH-D and IgE and a
threshold effect with both low and high 25-OH-D levels associated with elevated IgE
concentrations [69].
Main limitation to the present available data remain the use of indirect indicator, such as
VitD intake during pregnancy or estimated intakes based on dietary questionnaires to test a
causal relationship between VitD status and AD in children and the lack of randomised
controlled studies in children to prove the efficacy of VitD in preventing and treating allergic
skin diseases.
Vitamin D and Genetics

Genetic factors are undisputed determinants of different, individual response to VitD
exposure especially in early life. As effects of VitD are primarily mediated through VDRs,
single base variant genes have been investigated as risk factors for allergic diseases. In a cross
sectional study, Wjst analysed 13 Single Nucleotide Polymorphisms (SNPs) in the VDRs
gene obtained from 951 individuals belonging to 224 different lines of descents with at least 2
asthmatic children and altogether providing 11.383 genotypes [70]. In unaffected siblings, the
expression of specific VDR-SNPs was more pronounced, resulting from an “excess of
transmission”, demonstrated independently from age. The SNPs prevailing in the unaffected
group
also showed to be inversely related with a quantitative measure of the bronchial hyper-
reactivity, calculated through the analysis of the slope of the dose-response curve in a
standardised methacoline challenge protocol. It was thus proposed that the preferential
transmission of some particular VDRs variants could possibly be protecting against asthma
rather than predisposing to the disease.
SNPs were also tested to examine whether well-established genetic variants could modify
the relationship between a VitD deficient status (VDD) and food sensitisation (FS). VDD was
assessed in cord blood and defined as 25-OH-D < 11 ng/ml, whereas specific IgE ≥ 0.35
kUA/l to any of eight common food allergens in early childhood were used as a cut-off to
define FS.
SNPs were analysed among 11 genes including: molecules critical to the synthesis and
regulation of plasma IgE; genes encoding for the interleukin-4 and interleukin-13 (IL4 and
IL13) and their receptors (IL4R and IL13RA1), genes encoding the IgE receptor complex and
main genes encoding the molecules essential for 25-OH-D metabolism and regulation.
Results showed that VDD was associated with FS only when examined jointly with SNPs and
mainly referring to a particular IL4 gene polymorphism (rs2243250) supporting that VDD can
increase the risk of FS only among individuals with certain genotypes, and highlighting the
gene–vitamin D interaction on FS and athopic eczema [71]. It has been also speculated that
common rickets may derive, in the absence of proper endogenous VitD production, from a
genetically determined “low sensitivity” form, and allergy from a “high sensitivity” form, in
the presence of oral VitD exposure [72].
A preferential transmission of certain VDRs variants in children with allergic phenotype
and in unaffected can not be confirmed yet and further studies are needed to clarify this issue.
Conclusion
Vitamin D is the key element and the gold standard for the prevention and treatment of
rickets and osteomalacia.
Recent data prove that the spread practice of Vitamin D supplementation in early lives
has coincided with the rise of the allergic pandemic [15, 16, 68]. Contemporarily, there’s a
growing evidence supporting VitD to exert immune modulatory activities, conceivably
conferring protection against airways and gastrointestinal tract infections and providing anti
inflammatory benefits in humans. From one side, such virtues have been held up as
mechanisms, which possibly confer a VitD related benefit against the allergic march and
other allergic diseases. On the other hand, the VitD related Th2 increase observed in vitro has
focused the attention on cholecalciferol to be possibly involved in the development of the
allergic phenotype in genetically predisposed individuals. However, there’s no univocal
statement about this issue. As the impact of rickets on global health has been dramatically
reduced by the introduction of VitD supplementation, and being major guidelines established
according to bone health outcomes, randomised controlled trials are needed to clarify
secondary effects related to VitD supplements. Indeed, the first few months of life seem to be
particularly immunologically impressionable and the impact of an early supplementation with
VitD on the immune system and allergic phenotype development has not yet been examined.
Genetic predisposition and family history along with the entire amount of all possible
unknown interfering factors impacting on the individual answer to a standardised intervention
need to be further investigated to guarantee benefits other than that proved for bone health
and metabolism.
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Chapter VI
Factors Associated with Overweight

and Obesity among Kuwaiti
Young Children
A. N. Al-Isa1, Nadeeja Wijesekara2,

Ediriweera Desapriya3 and Yamesha Ranatunga4
1
Department of Community Medicine and Behavioral Sciences,
Faculty of Medicine, University of Kuwait, Kuwait City, Kuwait
2
Department of Medical Genetics, Centre for Molecular Medicine, and Therapeutics,
Child and Family Research Institute, University of British Columbia,
Vancouver, British Columbia, Canada
3
Department of Pediatrics, Faculty of Medicine, University of British Columbia,
4
Department of Food Nutrition and Health, University of British Columbia,
Abstract
Background. Childhood obesity is becoming a global epidemic which may result in
increased morbidity and mortality during young adulthood. Objectives. To identify
common factors associated with overweight and obesity among Kuwaiti intermediate
school children aged 10-14 years to support Kuwaiti obesity prevention policy making.
Methods. Weights and heights of 343 female and 340 male students were collected to
obtain body mass index (BMI). Results. The prevalence of overweight and obesity were
21.9 and 6.4% among females and 22.9 and 7.6% among males, respectively. Risk
factors for obesity in males and females vary considerably and also differ between age
groups. Conclusion. Health education programs focused on reducing obesity in Kuwait
must be multifactorial in nature and should be defined by gender and age group.

Correspondence should be addressed to Ediriweera Desapriya edesap@cw.bc.ca T. 604 875 2000 Ext.6707, F. 604
875 3569.
122 A. N. Al-Isa, N. Wijesekara, E. Desapriya et al.
1. Introduction
The widespread increase in the prevalence of overweight and obesity is a matter of great
concern. The serious health, social and economic impacts of this major public health issue led
the World Health Organization to recommend the continued surveillance of the population's
prevalence of obesity, using body mass index (BMI) as the indicator [1]. The fundamental
cause of weight gain is energy intake that persistently exceeds energy expenditure. However,
obesity is considered to be the result of a heterogeneous group of conditions, including
physical, social and behavioral elements [1]. Current prevalence and time trends in obesity
seem to reflect changing lifestyles in a changing environment. To further this, it has been
assumed that easy access to highly palatable foods induced excess consumption and that
obesity is due to lack of food avoidance by affected subjects [2, 3]. Regardless of cause,
obesity is a major public health concern primarily due to its well-recognized association with
important chronic disease conditions, including heart disease, stroke, diabetes, hypertension,
elevated blood lipids, osteoarthritis, and cancer [1].
Childhood obesity, defined as BMI greater than or equal to the 95th percentile is
currently on the rise in its prevalence world-wide. Same risk factors apply here, although the
greatest risk factor is considered as obesity of the parents. The issue of childhood obesity in
the Middle East, Kuwait in particular, will be addressed in this paper.
Among children, family history of obesity, diet, physical activity and mother’s education
have significantly correlated the development of obesity in the United Arab Emirates [4]. A
previous study of primary age (6-10 years) males in Kuwait determined that there were a
variety of additional factors associated with overweight and obesity; however, having one or
more obese brothers, an unemployed father or a high (>11) number of persons living at home
were significantly associated with higher risk of overweight and obesity. Increased age and
school level as well as having a chronic disease were associated with risk of overweight in
primary age males [5].
The purpose of this study was to explore the specific factors that are associated with
overweight and obesity among Kuwaiti intermediate school children aged 10-14 years to
determine if similar factors can be identified between males and females. The results will also
be compared to those of the primary age group to determine implications for obesity
prevention policy.
2. Methods
2.1. Sample
The sample comprised of 343 female and 340 male intermediate school pupils aged 10-
14 years drawn from their respective schools. Each student was provided with an informed
consent form to be filled out by his/her parents and/or guardians. This form explained the
non-invasive nature of the study and detailed the procedures. Only students whose caregivers
provided informed consent were included in this study.
Factors Associated with Overweight and Obesity among Kuwaiti Young Children 123
2.2. Measurements
The three primary measurements taken for this study were age, weight and height. Age
was ascertained to the nearest month from the pupil’s civil identification card which was
obtained from the school files containing the student’s date of birth.
Weight was measured by the author, with the student standing and wearing light clothes
to the nearest 0.1 kg, using a precalibrated digital SECA scale which was recalibrated
between measurements. Height was measured while the subject was standing without shoes to
the nearest 0.1 cm, using a specially designed portable stadiometer with a spirit level to
ensure that it was parallel to the flat hard floor during measurement. The BMI, which is the
weight in kilograms divided by the height in meters squared (kg/m2), was used as the index of
adiposity.
2.3. Data analysis
The Statistical Programme for the Social Sciences (SPSS) version 17, PC Windows was
used for data analysis. In addition to descriptive statistics, the 2 test was used to assess the
association between categorical variables. Logistic regression analysis was carried out using a
binary variable: non-obese (BMI <25kg/m2) or overweight [(BMI >25kg/m2)/obese (BMI >30
kg/m2)] as a dependent variable and a number of other variables as independent variables.
The merit of the logistic regression approach is that it leads to the adjusted odd ratios
(estimated relative risk or RR) of the independent variables in relation to a reference group. A
p-value of <0.05 was the criterion of statistical significance.
2.4. Associated Factors
Age was divided into five categories 10, 11, 12, 13 and 14. The following domains were
broken into sub factors.
2.4.1. Dieting and nutrition

Number of major meals into three: 1,2,3; eating between meals into three: yes, no,
sometimes; dieting into three: yes, no, was; number of times dieted into four: none, low (1-2),
medium (3-4), high (≥5); dieting practice into five: on my own, through a consultant, relatives
and friends, through the mass media, does not apply; own nutritional knowledge into three:
weak, good, excellent; needing special diet to lose weight into three: yes, no, do not know.
2.4.2. Activities and Interests

Practice sports (months per year) into three: 1 (< month), 2 (1-3 months), 3 (>9 months);
sport involvement (hours per week) into four: high (≥5), medium (3-4), low (≤2), none;
exercising into two: yes, no; countries preferred for visiting into four: western, eastern, both,
neither.
2.4.3. Socioeconomics
Type of housing into three: rent, government, private; number of rooms in the house into
three: low (1-2), medium (3-4) and high (≥5); number of those living at home into four: none
(0), low (1-2), medium (3-5), high (≥6); number of servants at home into four: none (0), low
(1-2), medium (3-5), high (≥6); family income per month into three: low (< 1500 $), medium
($1500 - $3000), high (>$3000).
2.4.4. Family
Number of brothers, sisters and total siblings into four: none (0), low (1-3), medium (4-
7), high (≥8); birth order into three: first, middle, last; number of obese brothers/sisters into
four: none (0), low (1-2), medium (3-4), high (≥5); obesity among first degree relatives into
four: none (0), low (1-2), medium (3-4), high (≥5); parental obesity into four: neither, father,
mother, both; parental education into three: low (illiterate or elementary), medium
(intermediate or secondary), high (college or higher); father’s employment status into two:
working, not working; relation between parents into three: first cousin, there is, there is not.
2.4.5. Academics
Current grade point average (GPA) into three: high (excellent and very good); medium
(good), low (low pass and failure); level of education into four: first, second, third, and fourth
year; high school studies into two: science, non-science; highest desired degree into three:
high school, college, higher.
2.4.6. Health
Dental status into three: healthy, treated by dentist, unhealthy; suffering from a chronic
disease into two: yes, no; last dental or physical check-up into four: do not remember, more
than two years, a year ago, a month ago; describe your health into three: bad, good, excellent;
feeling tired often into two: yes, no.
3. Results
The prevalence of being overweight and obese were 21.9 and 6.4% among females and
22.9 and 7.6% among males, respectively.
Table 1 and 2 show the factors associated with being overweight (BMI>25-30 Kg/m²)
and with obesity (BMI>30 Kg/m²) among Kuwaiti intermediate school children aged 10-14
years from a chi-squared analysis of female and male data. For females these factors were age
(p<0.05), number of brothers (p<0.01), number of obese brothers (p<0.01), number of meals
per day (p<0.05), number of persons living at home (p<0.01), number of servants (p<0.01),
monthly family income (p<0.05), sport involvement (hours per week) (p<0.05), high school
subjects (p<0.05), dieting (p<0.05), level of intermediate education (p<0.01), number of times
dieted (p<0.01) and diet consultation (p<0.001). For males these factors included number of
obese brothers (p<0.01), parental obesity (p<0.05), current GPA (p<0.05), last health check-
up (p<0.05), dieting (p<0.01), level of intermediate education (p<0.01), self-reported health
(p<0.05), number of times dieted (p<0.001), diet consultation (p<0.05) and needing special
nutrition program. Table 2 and 3 show the risk factors associated with being overweight
(BMI>25-30 Kg/m²) and with obesity (BMI>30 Kg/m²) among the same group of students
from logistic regression. In the female cohort, the risk of being overweight increased with
having no brothers (p<0.05, OR=7.0) in comparison with the reference group who had the
most number (≥5) of brothers, decreased among those who did not diet (p<0.05, OR=0.47) in
comparison with those in the reference group who dieted, decreased among those in the third
(p<0.01, OR=0.34) and fourth level of intermediate education (p<0.05, OR=0.42) in
comparison with the reference group in the first level, increased among those with low (1)
number of obese sisters (p<0.01, OR=2.75) in comparison with those in the reference group
who had none, and decreased among those who did not need a special nutrition program in
Table 1. Factors associated with overweight (BMI>25-30 kg/m2) and obesity

(BMI>30 kg/m2) among Kuwaiti intermediate female school children aged
10-14 years (n=343) from chi-squared analysis
Factor Non-obese Overweight Obese p-

value
n (%) n (%) n (%)
Age group (years) <0.05†
10 48 (19.5) 13 (17.3) 6 (27.3)
11 46 (18.7) 13 (17.3) 7 (31.8)
12 48 (19.5) 20 (26.7) 5 (22.7)
13 74 (30.1) 25 (33.4) 2 (9.1)
14 30 (12.2) 4 (5.3) 2 (9.1)
Number of brothers 0.01

High (>5) 14 95.7) 1 (1.3) 1 (4.5)
Medium (3-4) 57 (23.2) 13 (17.3) 10 (45.5)
n (%) n (%) n (%)
Low (1-2) 157 (63.8) 47 (62.7) 7 (31.8)
None 18 (7.3) 14 (18.7) 4 (18.2)
Number of obese brothers <0.01†

None 187 (76.0) 52 (69.3) 11 (50.0)
Low (1) 35 (14.2) 15 (20.0) 5 (22.7)
Medium (2) 21 (8.5) 6 (8.0) 5 (22.7)
High (3) 3 (1.2) 2 (2.7) 1 (4.5)
Number of meals per day <0.05

1 19 (7.7) 4 (5.3) 1 (4.5)
2 71 (28.9) 20 (26.7) 1 (4.5)
3 156 (63.4) 51 (68.0) 20 (90.9)
Number of persons living at 0.01

home
Low (<6) 91 (37.0) 37 (49.3) 2 (9.1)
Medium (7-10) 125 (50.8) 33 (44.0) 18 (81.8)
High (>11) 30 (12.2) 5 (6.7) 2 (9.1)
Table 1. (Continued)

value
n (%) n (%) n (%)
Number of servants <0.01
None 8 (3.3) 5 (6.7) 0 (0)
Low (1) 87 (35.8) 23 (30.7) 5 (22.7)
Medium (2) 97 (39.4) 25 (33.3) 4 (18.2)
High (>3) 53 (21.5) 22 (29.3) 13 (59.1)
Monthly family income <0.05
Low (< 700 KD) 27 (11.0) 8 (10.7) 0 (0)
Medium (KD 700- 155 (63.0) 41 (54.7) 12 (54.5)
1500)
High (KD >1500) 64 (26.0) 26 (34.7) 10 (45.5)
Practice sports (hours/week) <0.05

None 21 (8.5) 8 (10.7) 0 (0)
1-2 hours/week 16 (6.5) 8 (10.7) 1 (4.5)
3-4 hours/week 119 (48.4) 37 (49.3) 16 (72.8)
5-6 hours/week 66 (26.8) 18 (24.0) 5 (22.7)
>6 hours/week 24 (9.8) 4 (5.3) 0 (0)
High school subjects <0.05

Science 157 (63.8) 58 (77.3) 10 (45.5)
Non-science 89 (36.2) 17 (22.7) 12 (54.5)
Dieting <0.05
Yes 37 (15.0) 19 (25.3) 5 (22.7)
No 189 (76.8) 43 (57.3) 15 (68.2)
I was 20 (8.1) 13 (17.3) 2 (9.1)
Level of intermediate studies <0.01

1 55 (22.4) 27 (36.0) 6 (27.3)
2 55 (22.4) 25 (33.3) 8 (36.4)
3 73 (29.7) 10 (13.3) 5 (22.7)
4 63 (25.6) 13 (17.3) 3 (13.6)
Number of times dieted <0.01

None 173 (70.3) 38 (50.7) 11 (50.0)
Low (1) 29 (11.8) 11 (14.7) 6 (27.3)
Medium (2-3) 27 (11.0) 19 (25.3) 3 (13.6)
High (>4) 17 (6.9) 7 (9.3) 2 (9.1)
Diet consultation <0.001

Personal 153 (62.2) 45 (60.0) 9 (40.9)
Professional 26 (10.6) 6 (8.0) 10 (45.5)
Friends/Relatives 41 (16.7) 14 (8.7) 3 (13.6)
None 26 (10.6) 10 (13.3) 0 (0)
Table 2. Factors associated with overweight (BMI>25-30 kg/m2) and obesity

(BMI>30 kg/m2) among Kuwaiti intermediate male school children aged
10-14 years (n=340) from chi-squared analysis

value
n (%) n (%) n (%)
Number of obese brothers <0.01

None 169 (71.6) 48 (61.5) 14 (53.8)
Low (1) 43 (18.2) 17 (21.8) 6 (23.1)
Medium (2) 17 (7.2) 9 (11.5) 3 (11.5)
High (>3) 7 (3.0) 4 (5.1) 3 (11.5)
Parental obesity <0.05
None 183 (77.5) 66(84.6) 21 (80.8)
Father 29 (12.3) 3 (3.8) 2 (7.7)
Mother 22 (9.3) 9 (11.5) 3 (11.5)
Both
Current GPA <0.05

High 50 (21.2) 23 (29.5) 10 (38.5)
Medium 73 (30.9) 26 (33.3) 6 (23.1)
Low 113 (47.9) 29 (37.2) 10 (38.5)
Last health checkup <0.05

A month ago 34 (14.4) 4 (5.1) 3 (11.5)
1 year before 20 (8.5) 5 (6.4) 2 (7.7)
2 years before 19 (8.1) 16 (20.5) 4 (15.4)
Don’t remember 163 (69.1) 53 (67.9) 17 (65.4)
Dieting <0.01
Yes 28 (11.9) 16 (20.5) 9 (34.6)
No 190 (80.5) 53 (67.9) 12 (46.2)
I was 18 (7.6) 9 (11.5) 5 (19.2)
Level of intermediate <0.01

education
1 70 (29.7) 17 (21.8) 2 (7.7)
2 57 (24.2) 21 (26.9) 7 (26.9)
3 57 (24.2) 20 (25.6) 5 (19.2)
4 52 (22.0) 20 (25.6) 12 (27.0)
Health status <0.05
Excellent 155 (65.7) 42 (53.8) 11 (42.3)
Good 73 (30.9) 28 (35.9) 11 (42.3)
Poor 8 (3.4) 8 (10.3) 4 (15.4)
Table 2. (Continued)

value
n (%) n (%) n (%)
Number of times dieted <0.001
High (>4) 12 (5.1) 5 (6.4) 4 (15.4)
Medium (2-3) 11 (4.7) 23 (29.5) 10 (38.5)
Low (1) 22 (9.3) 10 (12.8) 5 (19.2)
None 191 (80.9) 40 (51.3) 7 (26.9)
Diet consultation <0.05
Personal 142 (60.2) 44 (56.4) 14 (53.8)
Professional 21 (8.9) 7 (9.0) 6 (23.1)
Friends/Relatives 34 (14.4) 17 (21.8) 6 (23.1)
None 39 (16.5) 10 (12.8) 0 (0)
Needing special diet <0.001
program
Yes 56 (23.7) 28 (35.9) 16 (61.5)
No 110 (46.6) 30 (38.5) 3 (11.5)
I don’t know 70 (29.7) 20 (25.6) 7 (27.0)
comparison with those in the reference group who needed it. The risk of obesity (BMI>30
Kg/m²) decreased among those who were not obese (p<0.001, OR=0.15) in comparison with
the reference group who increased among those with medium GPA (p<0.05, OR=2.69) in
comparison with those in the reference group with high GPA, increased among those with
poor health status (p<0.05, OR=4.98) in comparison with those in the reference group with
excellent health status and increased among those seeking consultation for weight loss from
professionals (p<0.001, OR=6.87) in comparison with those in the reference group who did it
on their own.
In the male cohort, the risk of being overweight decreased with those having low current
GPA (p<0.05, OR=0.52) in comparison with the reference group with high GPA, decreased in
the last health check-up two years before (p<0.01, OR=5.11) in comparison with the
reference group who had it a month ago, decreased among those who did not diet (p<0.01,
OR=0.38) in comparison with the reference group who dieted, increased among those in the
second level of intermediate education (p<0.05, OR=2.08) and in the fourth level (p<0.01,
OR=2.60) in comparison with the reference group in the first level, increased among those
with poor health status (p<0.01, OR=3.57) in comparison with the reference group who had
an excellent health status, increased among those who had attempted dieting a medium
number (2-3) of times (p<0.01, OR=4.0) and decreased among those who did not diet at all
(p<0.05, OR=0.32) in comparison with the reference group who dieted the most (≥4),
decreased among those not needing a special nutrition program (p<0.001, OR=0.35) and
those who didn’t know they needed the program (p<0.05,OR=0.49) in comparison with the
reference group who needed it.
Table 3. Risk factors associated with overweight (BMI>25-30 kg/m2) and obesity
(BMI>30 kg/m2) among Kuwaiti intermediate female school children
aged 10-14 years (n=343) from logistic regression
Factors Overweight Obese

OR (95% CI) OR (95% CI)
# brothers
High (>5) (reference) 1.0 1.0
Medium (3-4) 2.83 (0.59-13.42) 2.14 (0.25-18.03)
Low (1-2) 2.41 (0.53-10.93) 0.52 (0.06-4.46)
None 7.00 (1.39-35.34)* 1.88 (0.00-0.00)
Current GPA
High (reference) 1.0 1.0
Medium 0.97 (0.58-1.63) 2.69 (1.01-7.1)*
Low 0.57 (0.26-1.22) 2.10 (0.59-7.49)
Dieting
Yes (reference) 1.0 1.0
OR (95% CI) OR (95% CI)
No 0.47 (0.26-0.85)* 0.72 (0.25-2.07)
I was 1.16 (0.49-2.68) 0.68 (0.12-3.69)
Level of intermediate education

1 (reference) 1.0 1.0
2 1.00 (0.54-1.84) 1.37 (0.45-4.12)
3 0.34 (0.16-0.69)** 0.82 (0.24-2.80)
4 0.42 (0.21-0.85)* 0.54 (0.13-2.23)
Health status
Excellent (reference) 1.0 1.0
Good 1.13 (0.68-1.91) 1.05 (0.01-1.18)
Poor 1.68 (0.53-5.34) 4.98 (0.38-2.84)*
Number of obese sisters

None (reference) 1.0 1.0
Low (1) 2.75 (1.37-5.52)** 2.63 (0.90-7.65)
Medium (2) 1.06 (0.33-3.42) 0.00 (0.00-0.00)
High (>3) 1.45 (0.26-8.09) 3.36 (0.37-30.51)
Diet consultation
Personal (reference) 1.0 1.0
Professional 1.74 (0.87-3.49) 0.72 (0.25-2.07)
Friends/Relatives 1.18 (0.61-2.23) 1.20 (0.31-4.58)
None 1.09 (0.49-2.40) 0.00 (0.00-0.00)
Needing special diet program

No 0.50 (0.28-0.88)* 0.56 (0.21-1.49)
I don’t know 0.62 (0.34-1.12) 0.51 (0.16-1.58)
*<0.05, **<0.01, ***<0.001, OR (Odds Ratio), CI (Confidence Interval).

Table 4. Risk factors associated with overweight (BMI>25-30 kg/m2) and obesity
(BMI>30 kg/m2) among Kuwaiti intermediate male school children aged
10-14 years (n=340) from logistic regression

OR (95% CI) OR (95% CI)
Number of obese brothers

Low (1) 1.49 (0.83-2.67) 0.24 (0.05-0.94)*
Medium (2) 1.97 (0.88-4.35) 0.37 (0.08-1.69)
High (>3) 2.09 (0.69-6.26) 0.42 (0.07-2.43)
Number of obese relatives

Low (1-2) 1.29 (0.70-2.37) 2.96 (1.14-7.74)*
Medium (3-4) 1.34 (0.68-2.64) 0.65 (0.13-3.18)
High (>5) 1.20 (0.64-2.26) 1.35 (0.42-4.29)
Current GPA
High (reference) 1.0 1.0
Medium 0.66 (0.32-1.11) 0.44 (0.15-1.27)
Low 0.52 (0.29-0.92)* 0.51 (0.20-1.29)
Number of servants
Low (1) 0.56 (0.23-1.14) 0.25 (0.06-0.94)*
Medium (2) 0.76 (0.30-1.90) 0.35 (0.09-0.94)*
High (>3) 0.64 (0.23-1.73) 0.61 (0.15-2.29)
Last health checkup

A month ago 1.0 1.0
(reference)
1 year before 1.39 (0.41-4.69) 1.01 (0.15-6.50)
2 years before 5.11 (1.83-14.28)** 1.45 (0.30-6.92)
Don’t remember 2.04 (0.86-4.83) 0.99 (0.28-3.56)
Dieting
No 0.38 (0.20-0.69)** 0.24 (0.09-0.61)**
I was 0.76 (0.31-1.86) 0.90 (0.27-2.98)
Level of intermediate education
1 (reference) 1.0 1.0
2 2.08 (1.03-4.17)* 3.90 (0.79-19.35)
3 1.86 (0.91-3.77) 2.83 (0.53-14.97)
4 2.60 (1.30-5.18)** 7.25 (1.57-33.45)**
Health status
Excellent (reference) 1.0 1.0
Good 1.50 (0.91-2.47) 1.95 (0.81-4.65)
Poor 3.57 (1.40-9.10)** 4.47 (1.27-15.66)*

OR (95% CI) OR (95% CI)
Number of times dieted
High (>4) (reference) 1.0 1.0
Medium (2-3) 4.00 (1.33-12.03)** 1.25 (0.34-4.57)
Low (1) 0.81 (0.27-2.41) 0.66 (0.15-2.80)
None 0.32 (0.12-0.80)* 0.13 (0.03-0.48)**
Diet consultation
Personal (reference) 1.0 1.0
Professional 1.55 (0.73-3.31) 2.85 (1.01-8.01)*
Friends/Relatives 1.57 (0.85-2.91) 1.56 (0.52-4.27)
None 0.64 (0.30-1.37) 0.00 (0.00-0.00)
Needing special diet program

No 0.35 (0.20-0.61)*** 0.11 (0.03-0.39)***
I don’t know 0.49 (0.27-0.88)* 0.40 (0.16-1.04)
*<0.05, **<0.01, ***<0.001, OR (Odds Ratio), CI (Confidence Interval).
The risk of obesity (BMI>30 Kg/m²) decreased among those with low (1) number of
obese brothers (p<0.05, OR=0.24) in comparison with the reference group who had none,
increased among those with low (1-2) number of obese relatives (p<0.05, OR=2.96) in
comparison with the reference group who had none, decreased among those with low
(p<0.05, OR=0.25) and medium (p<0.05, OR=0.35) number of servants in comparison with
those in the reference group who had none, decreased among those who did not diet (p<0.01,
OR=0.24) in comparison with those in the reference group who did, increased among those in
the fourth level of intermediate school (p<0.01, OR=7.25) in comparison with the reference
group in the first level, increased among those with poor health status (p<0.05, OR=4.47) in
comparison with those in the reference group with excellent health status, decreased among
those who never dieted (p<0.01, OR=0.13) in comparison with those in the reference group
who dieted frequently, increased among those who sought professionals for diet consultation
(p<0.05, OR=2.85) in comparison with those in the reference group who did it themselves
and decreased among those who did not need a special nutrition program (p<0.001, OR=0.11)
in comparison with those in the reference group who needed it.
4. Discussion
There is a plethora of factors that has been associated with childhood obesity; however,
this study was able to define certain factors that are found in both male and female Kuwaiti
groups: number of obese siblings, dieting, health status and level of education. When
subjected to logistic regression, among both males and females, those who were not dieting
and not requiring a special nutrition program had reduced prevalence of being overweight.
For females, the risk of being overweight increased with having no brothers and having obese
sisters, while it decreased among those in higher levels of education. In males, while the risk
of being overweight increased with higher level of education, poor health status, and number
of times they had dieted, the risk of being overweight decreased with low GPA and never
dieting. Obesity risk was high among those with a poor health status in both males and
females. Lower GPA was also a risk that increased obesity in females. For males, risk of
obesity increased with having more obese relatives, higher level of education and among
those who consulted professionals for weight management. The prevalence of obesity was
lower among male participants with fewer obese brothers, fewer servants, not dieting or never
dieted, and those who did not require a special nutrition program.
As apparent from our data, it is a common occurrence that obesity runs in the family as it
tends to be associated with genetics [6]. However, it is becoming apparent that genetics alone
cannot account for the increased prevalence of this pathophysioloigcal condition. In the
current study, while higher level of education reduced the risk of being overweight in
females, it increased the risk of being overweight and obese in males. Although one may
assume that with a higher level of education students become more aware of preventive
measures, there is also a likelihood of their studies occupying most of their time in higher
grades, thus preventing them from engaging in physical activity and encouraging unhealthy
eating habits, such as snacking. It is difficult to judge whether some factors are simply
consequences or actual determinants of the risk of overweight/obese. Poor health status may
simply prevent students from engaging in physical activity leading to the onset of obesity or
may ensue as a consequence of the obesity. As it is difficult to fathom that risk of obesity
reduces with not/never dieting, it may be that students at low risk of becoming overweight
never had the need to diet. Conversely, students may begin dieting and consulting
professionals for weight management only after the onset of obesity and therefore, these are
not risk factors for obesity.
Some of the associated factors for the 10-14 year old age group were also found in the 6-
10 year old age group of Kuwaiti children, providing a general idea of the common concerns
that need to be addressed. These factors include having obese siblings and poor health status.
From this study we can see that obesity is indeed multi-factorial in nature and may not be
caused by the same factors in each case; there are few consistent patterns for risk of obesity in
the studied cohorts. In fact, some of the risks can be conflicting in different groups.
Additional studies with larger sample sizes are required to obtain a clearer picture of the
factors contributing to obesity and being overweight in this age group.
A multitude of cultural factors are associated with detrimental dietary habits and
insufficient physical activity levels among Kuwaitis. These variables act as barriers in
implementing action plans to combat obesity, and should be taken into account when
proceeding with obesity awareness.
As an oil rich nation, Kuwait’s rapid economic development and high incomes have
facilitated means for sedentary lifestyles. The Kuwaiti population is becoming increasingly
dependent on vehicles for transportation, reducing travel by foot. In Kuwaiti households,
employment of servants such as maids, cooks, and drivers, minimizes the need to perform
daily household tasks. More time is spent watching television and using the internet [7].
These factors associated with wealth and higher standards of living, are conducive to
sedentary lifestyles.
Several barriers challenge the need for Kuwaitis to engage in regular physical activity.
Many Kuwaitis are discouraged by lack of knowledge or faulty assumptions and attitudes
concerning exercise [7]. The weather conditions in Kuwait, mainly hot and dry year round,
also are unfavorable for outdoor physical activity and unfortunately is encouraging for the
consumption of sugar sweetened cold soda beverages.
Kuwait’s dietary habits are not suitable for sedentary lifestyles that entail low caloric
expenditure. Traditional Kuwaiti food is rich; daily diets tend to be high in calories, and high
in fat [8]. Meals often consist of large servings of meat such as red meat, chicken, or seafood
as well as dairy products like cheese or full fat yogurt [9]. The nature of Kuwaiti dining must
also be considered when assessing dietary patterns. In the household, it is common to eat
meals together with family and with guests. Social gatherings and celebrations with extended
family and friends occur frequently [8]. During these occasions, food is a key focus. A lavish
feast offered to guests is an indication of affluence. As generosity is culturally valued, it can
be disrespectful to offer a subpar meal [8]. In addition, fast food has become a norm in
Kuwaiti society and should be considered as a factor contributing to the high daily caloric
intakes [8]. A combination of over consumption and insufficient physical activity means
caloric intake will exceed caloric expenditure, resulting in weight gain.
Any changes implemented to lifestyle behaviors would become effective only if cultural
and religious boundaries are considered. Religious teachings can be used to enforce behaviour
change. In the Islamic hadith (reports of the words and deeds of the Prophet Muhammad),
good health is considered a blessing. The hadith encourages involvement in sporting activities
that promote a healthy lifestyle and encourage family participation and unity. According to
Hamid (1993: 40), the Prophet (pbuh) stressed the importance of regular physical activity
[10]. Prophet Muhammad encouraged bodily wellness via dietary restrictions. The Prophetic
advice to eat only when hungry and to stop eating before becoming fully satiated is valuable
advice for today’s society.
Early experiences of proper eating and physical activity are important in establishing
healthy lifestyle habits later in life. Interestingly, it has been suggested that practices set at
infancy are more crucial than those set during school years in preventing obesity [11].
However, pre-adolescent years cannot completely be ignored and preventative measures still
need to be set in place. Therefore, schools should consider incorporating diet consultation as
well as physical education classes into their curriculum. Clear guidelines should be set on the
amount of physical activity requirement for children. Educational programs must be flexible
in their approach and ensure that all children are receiving relevant information. Programs
may have to be tailored to different age groups, genders and health and physical status of
students. Special consideration should be given towards female participation in sports because
the agenda is typically set by the boys, and girls may be excluded by their male peers.
Furthermore, at this pre-teen stage, a time when girls are starting to display their femininity,
there may be some resistance to sports. Schools also have a tendency to favour those who
display talent, which could discourage those who are not in high physical form from
participation. Interestingly, a study conducted with secondary school students in Ontario,
Canada suggests that providing an alternate room for physical activity would be beneficial
[12]. Weather conditions in Kuwait should be taken into consideration when designating
space for physical activity.
There is some belief that home environment is more important than school environment
in setting health habits in young children [13]. Reiterating this point, a study has found that
children gain more weight during the summer months than during school year [14]. Further,
children of overweight parents are at a higher risk of developing obesity as they not only
provide the genes, but also the social and behavioral settings, including the diet and should be
examined within the context of this study [15]. Therefore, in addition to educating the
children, educating the parents of healthy eating habits, importance of exercise and early
signs for recognition of weight gain and obesity is of vital importance. Recognizing obesity as
necessitating treatment could lead to early implementation of improved health habits.
Pediatricians should be encouraged to routinely discuss these issues with visiting parents.
They should work with schools and the community to decrease the availability of foods and
beverages with little nutritional value [16]. Parents should be encouraged to provide their
children more nutritious foods such as fruits vegetables and whole grains, and to limit sugar
sweetened beverages and fried fast food. Further, parents should allow for the development of
the child’s innate ability to regulate food intake from very early on, therefore, children
become aware of when they have consumed enough food. Family meal times should be
encouraged as this would allow parents to enforce healthy eating habits on children, while
preventing consumption of food from fast food restaurants.
Interestingly, studies have found direct links to fast food advertising and childhood
obesity, such that food advertising to children has been banned in a number of countries [17].
In addition, a study has found decreasing media use (i.e. television) without specifically
encouraging more active behaviors results in significantly lower BMI in children [18].
Therefore, limiting television viewing in young children may be beneficial in reducing
obesity. An exploration into these areas in Kuwaiti children would be highly useful.
Prioritization of academics over physical activity is becoming common; however, parents
should take care to encourage their children to engage in play activities in addition to walking
to school and engaging in chores at home.
In summary, focus should be placed on raising awareness of childhood obesity,
implementing healthy eating habits, reducing sedentary lifestyle and encouraging physical
activity, and monitoring weight gain in children, which would lead to early intervention. In
Kuwait, continuing to develop a National Physical Activity Plan [19] is the first step towards
integrating obesity awareness into society, but it is important to incorporate cultural and
demographic variables as has been shown in a study discussing adherence to lifestyle
measures in Kuwait [20, 21]. In light of the variations in risk factors and the demonstrated
strengths and weaknesses of intervention programs, we encourage the Kuwaiti government
and private organizations to pursue obesity programming that incorporates a variety of
approaches to best serve the needs of Kuwaiti children.
References
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preventing and managing the global epidemic. Report of a WHO consultation, No
authors listed.
[2] Rubenstein AH (2005). Obesity: a modern epidemic. Trans. Am. Clin. Climatol. Assoc.,
116:103-111.
[3] Jackson RT, Al-Mousa Z, Al-Raqua M, et al. (2001) Prevalence of coronary risk factors
in healthy adult Kuwaitis. International Journals of Food Sciences and Nutrition,
52:301-311.
[4] Moussa MA, Skaik MB, Selanes SB, Yaghy OY and Bin-Othman SA. (1994) Factors
associated with obesity in schoolchildren. International Journal of obesity and Related
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18(7):513-5.
[5] Al-Isa A, Campbell J, Desapriya E. (2011) Factors associated with overweight and
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[6] Bell CG, Walley AJ, Froguel P. The genetics of human obesity. Nat Rev Genet
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[7] Ramadan J, Vuori I, Lankenau B, Schmid T, and Pratt M. (2010) Developing a national
physical activity plan: the Kuwait example. Global Health Promotion, 17:52.
[8] Serour M, Alqhenaei H, Al-Saqabi S, Mustafa AR and Ben-Nakhi A. (2007) Cultural
factors and patients' adherence to lifestyle measures. British J of General Practice,
57(537):291-5.
[9] Kandela P. (1999) The Kuwaiti passion for food cannot be shaken. The Lancet,
353:1249.
[10] Hamid AW. (1993) Islam the Natural Way. Maraisburg: Asmara Distributors.
[11] Dattilo AM, Birch L, Krebs NF, Lake A, Taveras EM, Saavedra J. (2012) Need for
early interventions in the prevention of pediatric overweight: Review and upcoming
directions. Journal of Obesity.
[12] Hobin EP, Leatherdale ST, Manske S, Dubin JA, Elliott S, Veugelers P. (2012) A
multilevel examination of gender differences in the association between features of the
school environment and physical activity among a sample of grades 9 to 12 students in
Ontario, Canada. BMC Public Health, 12(1):74.
[13] van Hook J, Altman CE. (2012) Competitive Food Sales in Schools and Childhood
Obesity: A Longitudinal Study. Sociology of Education, 85(1):23-39.
[14] Von Hippel PT, Powell B, Downey DB, Rowland NJ. (2007) The Effect of School on
Overweight in Childhood: Gain in Body Mass Index during the School Year and during
Summer Vacation. American Journal of Public Health, 97:696-702.
[15] Price RA, Stunkard AJ, Ness R et al. Childhood onset (age less than 10) obesity has
high familial risk. Int. J. Obes. 1990;14:185-95.
[16] American Academy of Pediatrics. (2003) Prevention of Pediatric Overweight and
Obesity Pediatrics, 112(2):424-30.
[17] Alkharfy KM. (2011) Food advertisements: to ban or not to ban? Ann. Saudi Med.,
31(6):567-8.
[18] Robinson T. Reducing children’s television viewing to prevent obesity: a randomized
controlled trial. JAMA, 1999;282:1561–1567.
[19] Ramadan J, Vuori I, Lankenau B, Schmid T, and Pratt M. (2010) Developing a national
physical activity plan: the Kuwait example. Global Health Promotion, 17:52.
[20] Serour M, Alqhenaei H, Al-Saqabi S, Mustafa AR and Ben-Nakhi A. (2007) Cultural
factors and patients' adherence to lifestyle measures. British J. of General Practice,
57(537):291-5.
[21] Naser Al-Isa A, Campbell J, Desapriya E. (2011) Factors Associated With Overweight
and Obesity Among Kuwaiti Men. Asia Pac. J. Public Health, Jun 28, 2011. [Epub
ahead of print].
Index
age, vii, viii, x, 1, 2, 3, 4, 7, 8, 9, 13, 14, 15, 20, 21,

# 22, 23, 24, 30, 39, 45, 46, 47, 49, 50, 51, 52, 53,
54, 55, 56, 64, 67, 69, 75, 77, 91, 92, 93, 96, 100,
21st century, 34
103, 110, 111, 112, 113, 114, 119, 121, 122, 123,
124, 132, 133, 135
A agencies, 69
aggressive therapy, 21
academic performance, ix, 89, 91, 103, 104 aging process, 57
acceptable daily intake (ADI), ix, 68, 73, 74, 84 agriculture, 70
access, 3, 65, 122 airways, 115
achondroplasia, 14 albumin, 9, 10, 12, 16, 28, 38
acid, viii, 59, 67, 73, 76, 79, 80, 83, 86, 111 alcohol consumption, 102
acidic, 17, 31 allergens, x, 12, 107, 108, 115, 116
acromion, 8 allergic reaction, 75
activity level, 6, 13 allergic rhinitis, 112
acute leukemia, 2, 42 allergy, vii, x, 42, 107, 108, 111, 112, 113, 114, 115,
acute lymphoblastic leukemia, 6, 34, 37, 38 116, 117, 119
acute myelogenous leukemia, 6 altered taste, vii, 1, 15
AD, 113, 114 alternative medicine, 63
ADA, 35 alters, 118
additives, 69, 72, 74, 75, 76, 77, 81, 83, 84, 86 amenorrhea, 24
adipose, 16 American Heart Association, 103
adipose tissue, 16 amino, 18, 25
adiposity, 102, 123 amino acid(s), 18, 25
adjustment, 18 ammonia, 22
adolescents, vii, viii, 1, 2, 4, 7, 8, 9, 16, 20, 30, 31, anemia, 11, 38
33, 34, 35, 36, 37, 45, 46, 50, 59, 60, 61, 63, 65, angioedema, 119
91, 99, 101, 102, 103, 104, 105, 116 anorexia, 25, 26
ADP, 6, 9 antibiotic, 18
adulthood, x, 91, 103, 112, 116, 121 anti-cancer, 12, 17, 26
adults, vii, ix, 1, 4, 7, 24, 35, 38, 45, 47, 49, 52, 58, antiemetics, 33
68, 103, 104, 107, 108, 112, 113, 118, 119 antigen, 12, 109, 110, 114
adverse effects, viii, 2, 28, 31, 46, 47, 57, 58, 69, 72 anxiety, 24
advertisements, 97, 135 apoptosis, 113, 118
affluence, 132 appetite, vii, ix, 1, 4, 23, 25, 28, 31, 33, 89, 95, 96
Africa, 2, 3 arthralgia, 24
African-American, 101, 104 arthritis, 116
ascites, 6, 17
138 Index
Asia, v, vii, viii, 43, 44, 45, 51, 56, 60, 62, 65, 104, body density, 9
135 body fat, 8, 36, 57, 58, 64
Asian Americans, 51 body mass index (BMI), x, 6, 7, 36, 39, 64, 91, 92,
Asian countries, viii, 44 101, 102, 104, 121, 122
assessment, vii, 1, 4, 5, 6, 8, 11, 12, 13, 30, 35, 36, body size, 5, 45, 64
37, 39, 68, 71, 72, 73, 76, 83, 84, 87 body weight, 4, 8, 9, 20, 21, 36, 47, 50, 57, 58, 68,
asthma, x, 85, 107, 108, 110, 111, 112, 115, 116, 72, 75, 76, 77, 79, 83, 104
117, 118, 119 bone, viii, 9, 11, 23, 38, 40, 41, 43, 44, 45, 46, 49,
asthmatic children, 87, 112, 114 50, 55, 56, 57, 59, 60, 61, 62, 63, 64, 65, 108, 115
ataxia, 24 bone marrow, 11, 38, 40, 41
atopic dermatitis, 113, 117, 119 bone marrow transplant, 38, 40, 41
atopic eczema, 111, 114 bone mass, 45, 56, 57, 59, 60, 61, 64, 65
atopy, 112, 118, 119 bone mineral content, 9, 62
attitudes, ix, 63, 89, 132 bone resorption, 56
authority, 70 boosters, 31
autologous bone marrow transplant, 38 bowel, 23, 24, 32
avoidance, 59, 122 brain, 2, 6
awareness, 68, 132, 134 brain tumor, 2, 6
breakdown, 12, 20
breastfeeding, 30, 52, 53, 63
B bronchial epithelial cells, 112
bronchoscopy, 113
bacteremia, 41
brothers, 122, 124, 125, 127, 128, 129, 131
bacteria, 17, 18, 27, 28, 31, 32, 70, 74
bad habits, 99
ban, 84, 135 C
Bangladesh, 56, 63
barriers, ix, 60, 89, 92, 132 cabbage, 32, 59
base, 58, 74, 114 cachexia, vii, 2, 4, 6, 15, 16
beef, 29, 102 caffeine, 32
beer, 26 calcium, vii, viii, 23, 28, 43, 44, 45, 46, 47, 48, 49,
behaviors, 101, 102, 103, 104, 133 50, 51, 52, 53, 55, 56, 57, 58, 59, 60, 61, 62, 63,
Beijing, 45, 52, 61 64, 65, 91, 101, 108, 110, 116, 118
beneficial effect, 56 calcium carbonate, 53, 55, 56, 59, 65
benefits, viii, ix, 43, 45, 60, 70, 107, 113, 115 calcium gluconate, viii, 44, 55
beverages, 33, 51, 64, 68, 76, 79, 104, 132, 133 calcium supplements, viii, 43, 44, 45, 52, 53, 55, 56,
BIA, 8 57, 58, 59, 63, 65
bias, 9 caloric intake, 132
bile, 5, 13 calorie, 13, 19, 39
bile duct, 5 calorimetry, 19, 20, 40
bilirubin, 16, 28 cancer, vii, viii, 1, 2, 3, 4, 6, 9, 10, 11, 12, 15, 16, 18,
bioavailability, 47, 56, 59, 60, 63, 65 20, 23, 25, 28, 29, 30, 32, 34, 35, 36, 38, 39, 41,
birth weight, 42 42, 122
Blacks, 2 cancer cachexia, vii, 2, 15, 16
bleeding, 24 cancer therapy, vii, 1
blood, 9, 10, 11, 16, 17, 21, 23, 25, 28, 40, 101, 110, capillary, 22
111, 112, 115, 118, 122 carbon, 19
blood cultures, 25 carbon dioxide, 19
blood urea nitrogen, 16, 21 caregivers, 5, 13, 122
blood vessels, 17 catabolism, 11, 16
bloodstream, 17 category a, 78
BMI, x, 6, 7, 8, 13, 14, 15, 35, 91, 98, 102, 103, 121, category b, 26
122, 123, 124, 125, 127, 128, 129, 131, 133 Caucasian population, 46
body composition, 5, 6, 7, 8, 9, 16, 36, 57, 64 causal relationship, 114
Index 139
CDC, 7, 13, 39 conflict, 94, 95

cell culture, 72 consensus, ix, 29, 39, 71, 107, 108
cell differentiation, 113 Consensus, 39
cell line(s), 117 consent, 92, 122
cerebral palsy, 14 constipation, vii, 1, 15
challenges, 34, 40 constituents, 62, 84
changing environment, 122 consulting, 132
cheese, 31, 59, 94, 110, 132 consumer protection, 67, 70, 85, 87
cheilosis, 6 consumers, 69, 70, 71, 74, 84, 85, 100, 102
chemical(s), viii, 67, 69, 70, 71, 72, 73, 74, 84, 85, consumption, ix, 11, 13, 25, 29, 45, 51, 52, 55, 57,
87 59, 62, 64, 69, 70, 74, 76, 84, 89, 90, 91, 92, 93,
chemokines, 109 94, 95, 96, 98, 99, 100, 101, 102, 103, 104, 111,
chemotherapy, vii, 1, 10, 11, 12, 15, 17, 18, 19, 22, 122, 132, 133
27, 35, 38, 41 consumption habits, 99
Chicago, 35, 39, 41 consumption patterns, 13, 69
chicken, 132 containers, 27
childhood, viii, 2, 15, 28, 30, 31, 34, 35, 36, 37, 42, contamination, 27
44, 56, 57, 59, 61, 62, 65, 68, 91, 92, 101, 102, controlled studies, 113, 114
103, 105, 110, 111, 113, 115, 116, 118, 122, 131, controlled trials, 55, 57, 58, 63, 113, 115
133, 134 controversial, ix, 107, 108, 109, 111
childhood cancer, 34, 35, 37, 42 cooking, 27
China, viii, 43, 48, 50, 51, 52, 53, 54, 55, 61, 62 cooperation, 84
cholecalciferol, 107, 109, 110, 111, 112, 113, 114, coping strategies, ix, 90
115 copper, 4, 23, 28, 31
cholelithiasis, 3 corticosteroid therapy, 20
cholesterol, 10, 109 corticosteroids, 10
chopping, 29 cost, 9, 20, 63, 84
chronic diseases, 68 cost effectiveness, 63
chronic illness, 6 Costa Rica, 112, 118
circulation, 13 creatine, 12
City, 117 creatinine, 11, 12, 22, 28, 39, 58
classes, 133 critical period, 59
classification, 16, 36 critical thinking, 4
cleaning, 32 cross sectional study, 114
clinical application, 41 cross-sectional study, 45
clinical trials, 40 CRP, 9
clothing, 7, 32 culture, 26
coding, 93 curriculum, 133
coefficient of variation, 7, 44, 47 CV, 44, 47
coffee, 95 cyclophosphamide, 19
cognitive performance, 103 cyclosporine, 17, 25
cognitive process, 103 cystic fibrosis, 36, 39
colitis, 4, 15, 30 cystitis, 19
colorectal cancer, 39 cytokines, 109
communication, 71, 84, 100
community(s), 52, 71, 112, 133
compliance, 100 D
complications, 3, 12, 17, 20, 24, 30, 37
data analysis, 92, 123
composition, 5, 9, 35, 37, 84, 103
data collection, ix, 5, 89, 92, 93
compounds, 73
decision-making process, 71
conceptualization, 34
defence, 110, 112, 114
conditioning, 17, 19
deficiency(s), ix, 4, 6, 7, 10, 11, 13, 18, 23, 31, 35,
confinement, 101
45, 46, 51, 56, 62, 107, 108, 112, 118, 119
140 Index
deficit, 4 dysuria, 19
degradation, 10
dehydration, 8, 10, 18, 32
dendritic cell, 117 E
dental caries, 35
earnings, 70
dentist, 31, 32, 97, 124
ecology, 114
Department of Health and Human Services, 35
economic development, 132
dependent variable, 123
economic status, 53
depression, 6, 24, 33
eczema, 108, 110, 113, 114, 115, 118, 119
depth, 5
edema, 6, 17
detachment, 24
education, x, 28, 53, 60, 121, 122, 124, 127, 128,
detectable, 73, 110
129, 130, 131
developing countries, vii, 1, 2, 56
egg, 94, 98
developmental process, 68
elementary school, 103, 104
deviation, 77, 78
eligibility criteria, 92
diabetes, 3, 122
emission, 71
dialysis, 37, 38
employment, 124, 132
diarrhea, vii, 1, 4, 12, 15, 16, 17, 18, 20, 22, 23, 24,
employment status, 124
25, 27
encoding, 115
diet, viii, ix, 2, 5, 6, 12, 13, 17, 18, 27, 28, 29, 30, 32,
endangered, 70
33, 35, 42, 47, 57, 59, 60, 61, 65, 84, 85, 89, 90,
energy, vii, ix, 1, 4, 6, 15, 16, 17, 18, 19, 20, 21, 22,
92, 100, 117, 122, 123, 124, 128, 129, 130, 131,
26, 28, 29, 31, 36, 37, 40, 57, 61, 63, 64, 89, 90,
132, 133
91, 94, 98, 103, 122
dietary fat, 13
energy density, 90, 103
Dietary Guidelines, 62
energy expenditure, 19, 20, 40, 57, 122
dietary habits, 44, 51, 132
enforcement, 69, 100
dietary intake, viii, 12, 13, 23, 38, 39, 44, 57, 60, 61,
enlargement, 6, 7
67, 75
environment(s), 13, 70, 100, 108, 116, 133, 135
dietary supplementation, viii, 43, 52
environmental factors, 68
dieting, 33, 105, 123, 124, 128, 131, 132
enzyme(s), 18, 109, 114
digestion, 5, 18
eosinophil count, 112
digestive enzymes, 18
eosinophilia, 117
discomfort, 17
epidemic, x, 90, 121, 134
discrimination, 101
epidemiology, 40, 42, 60, 72
disease-related death, vii, 1, 2, 30
epithelial ovarian cancer, 40
diseases, ix, 44, 107, 108, 111, 113, 114, 115, 116,
ergocalciferol, 109
117
essential fatty acids, 22
displacement, 6, 9
estimated daily intake (EDI), ix, 68, 76, 84
distribution, 3, 53
ethics, 92
dizziness, 24
ethnic diversity, 51
DNA, 108
ethnic groups, 45, 46, 51
doctors, 60
etiology, 63
dogs, 26, 76, 77
EU, 69, 73
DOI, 104
Europe, 38, 51, 56, 104
dominance, 110
European Commission, 58
dosage, 28, 47, 54, 56
European Community, 61
dose-response relationship, 72
European Union, 48, 50, 85
dosing, 3
everyday life, 108
Down syndrome, 14, 30
evidence, viii, ix, x, 26, 44, 45, 47, 50, 56, 57, 58,
drawing, 10
59, 64, 68, 86, 89, 91, 102, 107, 108, 109, 110,
drinking water, 72, 85
115
drug metabolism, 3, 30
excretion, 11, 12, 46, 58
drugs, 3, 17, 86
exercise, 60, 132, 133
Index 141
experimental autoimmune encephalomyelitis, 117 fraud, 69, 86

expertise, 84 fresco, 27
exposure, vii, viii, ix, 9, 12, 17, 23, 30, 67, 68, 69, fructose, 90
70, 71, 72, 73, 74, 75, 76, 77, 81, 83, 84, 85, 87, fruits, 29, 31, 76, 133
101, 108, 109, 110, 111, 114, 115 FTIR, 9
fungal infection, 18
fungi, 74
F
facilitators, ix, 89, 92 G

failure to thrive, 20
false negative, 12 gallbladder, 5
families, vii, ix, 44, 89, 91, 92, 93, 96, 99 gastrointestinal tract, 16, 114, 115
family environment, 91 gender differences, 135
family history, 115, 122 gene expression, 117, 118
family income, 53, 123, 124, 126 genes, 109, 114, 115, 133
fast food, 132, 133 genetic mutations, 13
fasting, 10 genetic predisposition, 2, 100, 108
fat, 6, 7, 9, 10, 13, 15, 18, 22, 32, 37, 57, 78, 97, 100, genetics, 131, 134
102, 105, 110, 111, 132 gestation, 14
fat intake, 22 gestational age, 64
fat soluble, 22 global health, ix, 107, 115
fatty acids, 26, 111 glossitis, 6
fear, 94 glucocorticoids, 10, 112
femininity, 133 glucose, 9, 10, 38
ferritin, 11, 38 glucose tolerance, 38
fever, 20, 22, 24, 25 glutamine, 18, 25, 40, 41
fiber, 32, 101 GPA, 124, 127, 128, 130, 131
fights, 95 grades, 131, 135
Finland, 111, 116 gravity, 112
first degree relative, 124 growth, vii, 1, 4, 7, 8, 13, 14, 20, 22, 23, 26, 27, 35,
fish, 26, 27, 29, 31, 53, 111, 118 36, 39, 49, 50, 55, 59, 61, 64, 68, 74, 101, 108,
fish oil, 53 109
fistulas, 22 Guatemala, 34
flame, 29 guidance, 47, 92, 101
flora, 18 guidelines, ix, 17, 18, 26, 29, 37, 39, 42, 84, 107,
fluid, 7, 8, 9, 17, 18, 21, 22, 56 115, 133
focus groups, 93
folate, 30, 97
food additive(s), ix, 67, 70, 71, 72, 74, 75, 76, 77, 78, H
84, 85, 86, 87
hair, 6, 119
Food and Drug Administration, 85
hair follicle, 119
food industry, 70, 84
half-life, 3, 10, 21
food intake, viii, ix, 13, 25, 33, 67, 77, 89, 133
Hawaii, 60
food poisoning, 69, 74
hazards, 70, 72
food production, 70, 74
headache, 24
food products, 68, 69, 74, 78, 83, 84
healing, 4, 6, 25, 30
food safety, 26, 28, 70, 74, 84, 85, 87
health, vii, viii, ix, 23, 34, 37, 43, 44, 45, 47, 50, 52,
food security, 87
58, 59, 60, 61, 62, 63, 64, 68, 70, 71, 72, 73, 74,
formation, 46, 61
75, 84, 85, 87, 89, 91, 92, 100, 101, 102, 103,
formula, viii, 12, 14, 44, 46, 47, 49, 55, 58, 59, 65,
107, 108, 115, 122, 124, 127, 128, 130, 131, 132,
112
133
fractures, 56, 59, 63, 64
health care, 45
fragility, 59
142 Index
health effects, 47, 50, 72, 73

health risks, 70, 87
I
health status, 73, 125, 128, 131, 132
iatrogenic, 11
heart disease, 122
ideal, 8, 12, 36, 98
heartburn, 17, 23, 32
identification, 72, 84, 123
heavy metals, 70
idiopathic, 113, 116
height, viii, 6, 7, 8, 11, 12, 13, 14, 15, 20, 39, 64, 67,
IL-13, 109
75, 91, 92, 123
immune function, 108, 114
height growth, 8
immune modulation, vii, 109
hematocrit, 9, 11
immune response, 109
hematuria, 19
immune system, 16, 18, 109, 110, 115, 117, 118
hemodialysis, 37
immunity, ix, 12, 107
hemoglobin, 9, 11
immunocompromised, vii, 2, 26
hepatic failure, 21
immunomodulatory, 118
hepatotoxicity, 24
improvements, 28
high income countries, vii, 1, 2, 3, 28, 30
in utero, 110
high school, 105, 124
in vitro, ix, 107, 109, 112, 114, 115
higher education, 55
in vivo, 110, 112, 113
historical data, 5
incidence, 2, 25, 33, 34, 44, 51, 58, 108, 110, 111,
history, 4, 6, 13, 23, 111
112
HIV, 118
income, vii, 1, 2, 3, 28, 30, 34, 54, 55, 63, 90, 92
HIV-1, 118
independent variable, 123
homeostasis, 16
India, 3, 56, 63
homes, 75, 93
individuals, ix, 7, 9, 46, 56, 89, 90, 91, 107, 114, 115
hormone, 10
inducer, 118
hospitalization, 12, 24
induction, 38, 118
host, 4, 28, 30, 40, 112
industrial revolution, 108
household income, viii, 43, 53, 55, 92
industrialisation, 108
household tasks, 132
industry, 64, 70, 74, 75
housing, 123
infancy, x, 44, 57, 59, 62, 107, 108, 117, 133
HSCT, 4, 6, 10, 11, 15, 16, 17, 18, 19, 20, 21, 24, 25,
infant feeding practices, 52
26, 27, 28
infants, viii, 5, 12, 13, 14, 18, 20, 22, 39, 43, 44, 45,
human, 9, 16, 46, 59, 61, 62, 69, 72, 73, 84, 85, 110,
46, 47, 48, 49, 50, 51, 52, 58, 59, 60, 61, 63, 64,
112, 117, 118, 134
65, 69, 71, 109, 110, 116, 118
human exposure, 73
infection, 3, 10, 16, 18, 19, 20, 24, 30, 111, 118
human health, 84, 85
inflammation, 4, 9, 11, 18, 19
human leukocyte antigen, 16
inflammatory mediators, 10, 109
human milk, 9, 46, 62
inflammatory responses, ix, 107, 112
human right(s), 69
informed consent, 122
hydrogen, 20
ingredients, 70, 74, 84
hyperalimentation, 12, 39
inheritance, 117
hypercalciuria, 58
inhibition, 109, 113
hyperglycemia, 10, 20, 26, 38
initiation, 26, 53
hyperlipidemia, 3, 26
injury(s), 18, 114
hyperphosphatemia, 18
innate immunity, 109, 112
hyperpnea, 24
insomnia, 24
hypersensitivity, 11, 12, 39
inspections, 78
hypertension, 3, 122
institutions, 26
hypertriglyceridemia, 11
insulin, 3, 10, 33, 38
hypophosphatemia, 26
insulin resistance, 3, 33
hypotension, 18
integration, 10, 73
hypothesis, 110, 113, 114, 116
integrity, 25
intensive care unit, 10, 37
Index 143
interference, 47 lifestyle changes, 108

intervention, viii, 14, 17, 30, 44, 56, 57, 58, 59, 90, lifetime, 68, 70, 72
115, 134 ligand, 108
intervention strategies, 90 light, 17, 71, 100, 123, 134
intestinal tract, 24 lipids, 122
introspection, 94 liquids, 29, 31, 32, 33
ionizing radiation, 9, 30 literacy, 100
iron, 11, 23, 47, 56, 57, 60, 62, 65, 97 liver, 5, 6, 10, 16, 17, 21, 22, 45, 109
irradiation, 17, 18, 22 liver cells, 109
Islam, 134 liver failure, 21, 22
isotope, 6, 9, 20 logistics, 95
issues, 13, 70, 85, 96, 97, 100, 133 longitudinal study, 61
Italy, 40, 107 loss of appetite, vii, 1, 4, 15, 30
love, 97
low risk, 27, 132
J low-density lipoprotein, 10
lower respiratory tract infection, 111, 118
Japan, 48, 51
lumbar spine, 58
jaundice, 16, 17, 24
lung function, 112, 118, 119
juvenile rheumatoid arthritis, 108
lupus, 108
lymph, 6
K lymph gland, 6
lymphocytes, 114
Kaposi sarcoma, 2 lymphoma, 2, 6
keratinocytes, 112, 114, 119 lysis, 18
kidney, 10, 58, 109
kidney failure, 10
M
kidney stones, 58
kindergarten, 52, 77, 84
macronutrients, 4, 17, 31
kindergartens, viii, 52, 67, 75, 84
macrophages, 18, 109, 110, 112, 118
kinetics, 61, 62
magnesium, 28, 56, 57, 97
Kuwait, x, 121, 122, 132, 133, 134, 135
magnitude, 72, 84
majority, 2, 69, 94
L malabsorption, 4, 10, 11, 13, 17, 18, 23, 45, 59, 60,
65
labeling, 102 malignancy, 38
lack of control, 96, 99 malignant cells, 11
lactase, 18, 44, 51, 60, 62 malnutrition, vii, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12,
lactase deficiency, 44, 51, 60, 62 13, 14, 15, 16, 18, 30, 35, 36, 38, 39
Lactobacillus, 18 management, viii, 2, 17, 28, 31, 39, 40, 71
lactose, 17, 18, 28, 32, 45, 59, 60, 65 manufacturing, 69, 85
lactose intolerance, 32, 45, 59, 60, 65 marital status, 53
large intestine, 5 marketing, 90, 97, 100, 103, 105
later life, 45, 57, 91 marrow, 27, 38, 40, 41
Latin America, 34 Maryland, 86, 87
LDL, 10 mass, x, 6, 7, 9, 12, 24, 37, 38, 57, 63, 91, 92, 102,
lead, 11, 18, 56, 58, 61, 65, 84, 108, 133, 134 113, 121, 122, 123
lean body mass, 8, 9, 11, 15, 16, 20, 37 mass media, 123
legislation, 69, 72 mass spectrometry, 9
leukemia, 4, 42 matter, 103, 122
level of education, 124, 131 MB, 134
life cycle, 72 measurement(s), viii, 6, 7, 8, 9, 11, 16, 40, 50, 64,
lifestyle behaviors, 132 67, 74, 75, 77, 123
144 Index
meat, 26, 29, 31, 74, 75, 77, 78, 79, 80, 83, 94, 132 negative outcomes, 95
mechanical ventilation, 40 neuroblastoma, 2, 4, 6
media, 133 neurosurgery, 38
median, 7, 46 neurotoxicity, 86
medical, 5, 6, 10, 34, 52, 65 neutropenia, 18, 31
medical history, 6 neutrophils, 18, 112
medication, 6, 7, 10, 18, 63 New England, 103
medicine, 6 New Zealand, 37, 47, 48, 55, 60, 62, 63, 102, 104
medulloblastoma, 6, 35 Nigeria, 56
mellitus, 116 nitrates, ix, 68, 79, 82, 83
menopause, 64, 65 nitrite, viii, 67, 76, 83
mental activity, ix, 89 nitrogen, 11, 16, 21, 22, 25, 38
meta analysis, 42 NK cells, 109
meta-analysis, 45, 55, 58, 63, 64, 65, 116 no voice, 68
Metabolic, 37, 38, 40, 134 normal development, 44
metabolic pathways, 68 North America, 35, 45, 51, 63
metabolic responses, 65 NPC, 21, 22
metabolism, 4, 11, 30, 46, 57, 61, 108, 115, 117, 118 nurses, 5
mice, 109, 112, 114, 119 nutrient(s), 2, 17, 18, 23, 24, 33, 46, 47, 48, 51, 55,
microcephaly, 15 57, 59, 60, 62, 63, 64, 74, 91, 97, 98, 100, 101,
micronutrients, 4, 7, 31, 50 102, 104
microorganisms, 70, 74 nutrition, vii, viii, ix, 2, 4, 5, 6, 7, 12, 17, 18, 21, 24,
Middle East, 122 25, 28, 30, 36, 37, 38, 39, 40, 41, 59, 60, 61, 62,
migration, 117 64, 65, 77, 84, 85, 89, 100, 102, 103, 104, 117,
milligrams, 69 123, 124, 128, 131
mineralization, 9, 45 nutrition labels, 100
MIP, 110 nutritional assessment, 4, 5, 6, 9, 10, 13, 37
mixing, 9 nutritional deficiencies, 35
modelling, 72, 73, 87, 99, 100 nutritional screening, 5
models, 109, 112, 114 nutritional status, vii, 1, 4, 5, 7, 8, 9, 10, 11, 12, 13,
modifications, vii, 1, 23 16, 23, 25, 30, 34, 36, 37, 38, 104
mold, 26 nutritional therapy, vii, 1, 4, 23
molecules, 108, 110, 115
mood change, 24
morbidity, x, 10, 37, 41, 121 O
morphine, 25
obesity, vii, ix, x, 2, 3, 4, 6, 14, 30, 34, 35, 64, 89,
mortality, x, 8, 10, 36, 37, 121
90, 92, 93, 99, 100, 101, 102, 103, 104, 105, 108,
mouth sores, vii, 1
116, 121, 122, 124, 125, 127, 128, 129, 131, 132,
mucous membrane(s), 6, 18
133, 134, 135
multiple sclerosis, 108, 116
obesity prevention, x, 121, 122
muscle mass, 8, 11, 12, 15, 16, 35
occupational asthma, 86
musculoskeletal, 16
occupational health, 70
musculoskeletal system, 16
OH, 28, 56, 60, 108, 109, 110, 111, 112, 113, 114,
mycobacteria, 112
115, 118
myeloid cells, 112
oil, 22, 45, 116, 132
myelosuppression, 11
old age, 50, 132
myocardial infarction, 58, 65
omega-3, 118
opportunities, viii, 2, 30, 31, 70
N organ(s), vii, 1, 4, 7, 16
orthostatic hypotension, 24
National Academy of Sciences, 49 osteoarthritis, 122
National Institutes of Health, 16, 39 osteomalacia, 115
nausea, vii, 1, 4, 15, 16, 17, 18, 20, 24, 27, 30, 33 osteoporosis, 23, 40, 44, 57, 59, 64, 65
Index 145
outpatient(s), 5, 7, 28, 41 policy making, x, 121

overlap, 16 pollution, 108
overnutrition, 2, 3, 30 polymorphism, 115
overweight, vii, ix, x, 14, 15, 89, 90, 91, 92, 93, 99, polyphosphates, vii, viii, ix, 67, 68, 73, 74, 75, 76,
102, 103, 104, 121, 122, 123, 124, 125, 127, 128, 78, 79, 80, 81, 82, 83, 84, 86
129, 131, 132, 133, 134 polyunsaturated fat, 111, 118
oxalate, 59 polyunsaturated fatty acids, 111, 118
oxygen, 19, 20 population, 2, 3, 12, 23, 25, 26, 37, 40, 46, 47, 50,
oxygen consumption, 19 51, 52, 57, 58, 64, 68, 69, 71, 74, 77, 85, 92, 102,
108, 110, 111, 112, 113, 114, 118, 122, 132
population group, 46, 50, 51
P positive correlation, 25
positive relationship, 113
Pacific, viii, 43, 45, 104
potassium, 6, 9, 28, 32, 97
pain, 5, 12, 17, 24, 31
poultry, 26, 29, 31
pancreas, 18
poverty, 103
pancreatic insufficiency, 18
Prader-Willi syndrome, 14
pancreatitis, 4, 15
pregnancy, 30, 42, 110, 111, 113, 114, 118, 119
parallel, 8, 123
preparation, 4, 27, 90, 91
parameter estimation, 73
preschool, vii, viii, 36, 64, 67, 68, 75, 76, 77, 84
parenting, 92, 96, 99
preschool children, vii, viii, 36, 64, 67, 68, 75, 76,
parents, viii, ix, 43, 45, 53, 59, 60, 69, 75, 77, 78, 84,
77, 84
85, 89, 90, 91, 92, 93, 94, 95, 98, 99, 100, 122,
preservative, ix, 68, 80, 83
124, 133, 134
President, 86
participants, 52, 84, 92-98, 100, 131
prevention, vii, x, 1, 4, 29, 30, 40, 45, 105, 107, 108,
pathogenesis, 108, 113
115, 116, 134
pathogens, 26, 70, 112
primary school, 62
pathophysiology, 112
principles, 9
pathways, 100
probability, 71
peptide, 112, 118
probiotics, 18, 31, 53
percentile, 14, 15, 20, 58, 122
producers, 68, 70
peripheral blood, 41
professionals, 7, 59, 60, 125, 131, 132
Perth, 43, 52, 53, 55, 63
profit, 70
petechiae, 6
prognosis, 6
pharyngitis, 24
prognostic implications, vii, 1, 3
phenotype(s), ix, 107, 108, 109, 110, 112, 115, 118
programming, 118, 134
Philadelphia, 34, 86
pro-inflammatory, 109, 118
phosphate, 58, 59, 74, 108
project, 39, 92, 102
phosphorus, 57, 65
proliferation, 109, 113
physical activity, viii, 2, 29, 45, 56, 91, 122, 131,
prophylaxis, 18, 108
132, 133, 134, 135
protection, 69, 70, 85, 115
physical education, 133
protective role, 108, 112
physical inactivity, 4, 30, 102
protein energy malnutrition, vii, 1, 4, 31
pilot study, 24, 40
protein synthesis, 10
placebo, 40, 41, 57, 58, 64, 113
proteins, 9, 10, 13, 22, 37, 108
placenta, 46, 110
pseudotumor cerebri, 3
plasma levels, 108, 113
psychiatrist, 33
plausibility, 72
psychological development, 3
playing, 108, 109, 110
puberty, 3, 61
plethysmography, 6, 36
public concern, 70
poison, 72
public health, viii, 44, 56, 58, 59, 70, 73, 103, 122
polarization, 110, 117
public policy, 93
policy, x, 92, 103, 121, 122
publishing, 62, 86
policy makers, 92
146 Index
pulmonary edema, 22 rights, 70

risk assessment, 68, 70, 71, 72, 73, 74, 77, 84, 85, 87
risk factors, 4, 57, 65, 102, 104, 114, 122, 124, 132,
Q 134
risk management, 70, 71, 84
quadriceps, 6
risks, viii, 3, 5, 43, 60, 68, 70, 132
questionnaire, 13, 52, 53, 58, 75, 77
room temperature, 27, 31, 32
routes, 69
R Royal Society, 85
rules, 98, 100
radiation, vii, 1, 12, 15, 17, 18, 19, 116 rural areas, 45
radiotherapy, 11
Ramadan, 134, 135
S
rash, 16, 113, 119
reactant, 11
safety, 18, 47, 59, 70, 72, 73, 74, 76, 83, 85, 87
reactants, 10
saliva, 9, 17, 32
reactions, 75, 86
school, x, 45, 52, 54, 59, 63, 94, 95, 99, 101, 102,
reactivity, 114
104, 121, 122, 123, 124, 125, 126, 127, 128, 129,
reality, 69, 94
131, 133, 134, 135
recall, 13
science, 67, 124, 126
receptors, 109, 115
seafood, 132
recognition, vii, 1, 4, 70, 90, 133
secondary school students, 133
recommendations, 23, 26, 29, 45, 46, 49, 73, 103,
secrete, 18
104
secretion, 10, 17, 38
recovery, 4, 11, 24, 30
sedentary lifestyle, 132, 134
recurrence, 29
selenium, 4, 23, 28, 31
red blood cells, 62
sensation(s), 25, 31
regions of the world, 51
sensitivity, 69, 73, 87, 109, 115
regression, 123, 124, 128, 129, 130, 131
sensitization, x, 107, 108, 118, 119
regression analysis, 123
serum, ix, 10, 11, 16, 22, 28, 37, 58, 107, 108, 112,
relapses, 25
113, 119
relatives, 123, 129, 131
serum albumin, 10, 16, 37
relevance, 93
serum ferritin, 11
remission, 38
services, 69
renal dysfunction, 17, 18
SES, 90, 91, 92, 93, 99, 100
renal failure, 21, 22
severe asthma, 113
rent, 123
sex, viii, 7, 13, 14, 46, 67
repair, 20
shelf life, 68, 74
requirements, 19, 20, 21, 23, 40, 45, 46, 47, 49, 50,
shock, 41
60, 61, 62, 92, 118
showing, 109
resale, 69
siblings, 114, 124, 131, 132
reserves, 8
side effects, vii, 1, 4, 15, 16, 17, 18, 30
resistance, 10, 133
signaling pathway, 119
resolution, 87
signs, 6, 15, 16, 133
resources, 4, 6, 34, 71
Singapore, 87
response, ix, 9, 10, 12, 21, 22, 39, 52, 69, 70, 72, 73,
sinusoidal obstruction syndrome, 17
87, 107, 109, 112, 114, 117, 119
skeletal muscle, 16
restaurants, 133
skeleton, 44, 46, 49, 57
restrictions, 5, 133
skin, 6, 8, 12, 15, 16, 17, 22, 35, 108, 109, 113, 114
retinoblastoma, 2
skin diseases, 113, 114
retinol, 9, 10
skinfolds, 8
rhinitis, 110
sleep apnea, 3
rickets, 45, 56, 59, 60, 63, 108, 109, 115, 116
smooth muscle, 113
Index 147
snacking, 33, 90, 104, 131 target population, 47, 72

society, 132, 133, 134 TDI, 73, 74, 86
socioeconomic status, ix, 13, 16, 89, 90, 102 teachers, 52
sodium, 29, 32 techniques, 4, 37
softener, 32 technology, 9, 87
solid tumors, 6, 11, 38 teens, 91
solution, 55 teeth, 6, 32, 97
South Africa, 87 telephone, 93
soymilk, 59, 65 television viewing, 133, 135
Spring, 64 tertiary education, 92
stability, 74 testing, 11, 103
staff members, 63 texture, 31, 74
stakeholders, 71, 84 Thailand, 62
standard deviation, 47 therapeutic benefits, 113
state, 10, 11, 16, 34, 101, 102 therapy, vii, viii, 1, 2, 3, 4, 7, 8, 17, 18, 21, 22, 23,
statistics, 33, 34, 123 28, 30, 37, 38, 39, 113
steatorrhea, 13, 18 threats, 70, 85
steroids, 17, 33, 108 thrombophlebitis, 24
stimulant, 28, 33 thyroid, 10
stomach, 16, 17, 24, 94 time commitment, 9
stomatitis, 6, 41 time constraints, ix, 89
storage, 12 tissue, 20, 28, 72, 109
strategy use, 95 TLR, 117
stress, 6, 16, 21, 73 tobacco, 29
stroke, 122 toddlers, 22, 39
structure, 72, 93, 112, 118 tofu, 59
style, 27 tooth, 35
sulphur, viii, 67, 79, 80, 81, 83, 85 total cholesterol, 10
supplementation, vii, viii, x, 12, 18, 23, 25, 41, 43, total energy, 22, 25
44, 45, 47, 52, 55, 56, 57, 58, 59, 61, 63, 64, 65, total parenteral nutrition, 11, 22, 25, 28, 40
107, 108, 109, 110, 111, 113, 115, 116, 119 toxicity, 25, 38, 39, 47, 69, 73
surface area, 9, 13, 22 toxicology, 72, 84, 85, 86
surveillance, 122 toxicology studies, 72
survival, vii, 1, 2, 3, 10, 25, 28, 30, 33, 109, 117 trade, 87, 96, 100
survival rate, vii, 1, 2, 28, 30 trade-off, 96, 100
survivors, 23, 29, 37, 42 traits, 109
susceptibility, 3, 16, 30, 68, 71, 119 transcription, 108
sweat, 9 transferrin, 9, 10, 11, 12, 38
sweeteners, 84 transformation, 7
swelling, 17 transfusion, 11, 23
Switzerland, 34 translocation, 25
symptoms, 4, 17, 23, 59, 110, 112, 113, 114, 118 transmission, 114, 115
syndrome, 14, 16, 18, 22, 26, 41 transplant, 18, 24, 28, 38, 40, 41, 42
synthesis, 10, 115 transplant recipients, 24, 38, 40
transplantation, vii, 1, 4, 16, 20, 24, 27, 30, 37, 40,
41
T transport, 13
transportation, 132
T cell(s), ix, 107, 109, 112, 117
trauma, 41
tachycardia, 24
treatment, vii, x, 1, 2, 3, 4, 9, 10, 11, 12, 16, 17, 18,
tactics, 70
20, 23, 25, 26, 28, 29, 30, 32, 34, 37, 107, 108,
Taiwan, 52
111, 113, 115, 116, 119, 133
talent, 133
trial, 40, 41, 64, 65, 119, 135
target, 47, 72, 108
148 Index
triceps, 6, 8, 36
triggers, 117, 118
W
triglycerides, 10
waking, ix, 89, 91
tuberculosis, 118
walking, 95, 134
tumor(s), 7, 18, 29, 42
Washington, 38, 40, 42, 61, 62, 65, 85, 86, 87
turgor, 22
waste, 17, 75
type 1 diabetes, 108, 116
water, 9, 19, 20, 27, 31, 32, 36, 74, 116
wealth, 132
U weaning infants, viii, 43, 44, 59
web, 42
UL, 44, 46, 47, 48, 50, 51, 58 weblog, 92
ultrasound, 64 weight changes, 22
UN, 21 weight control, 57
undernutrition, 2, 3, 15 weight gain, vii, ix, 1, 5, 14, 17, 23, 33, 57, 58, 64,
undesirable weight loss, vii, 1, 15 89, 103, 122, 132, 133, 134
uniform, 4, 96 weight loss, vii, 1, 5, 14, 15, 17, 26, 38, 125
United, vii, 1, 2, 13, 33, 34, 39, 44, 47, 48, 49, 61, weight management, 19, 91, 131, 132
85, 102, 122 weight reduction, 65
United Kingdom, 102 weight status, 91, 93, 100, 102
United Nations, 34, 44, 49, 61 well-being, 68
United States, vii, 1, 2, 13, 33, 34, 39, 44, 47-49, 85 wellness, 133
urban, 61, 62 Western Australia, 43, 63, 89
urban areas, 61, 62 Western countries, 108
urea, 11 Western Europe, 49
urine, 9, 11, 12, 22 wheeze, 110, 111, 113, 118, 119
urticaria, 75, 87, 113, 114, 119 wheezing, 110, 111, 118
US Department of Health and Human Services, 34 WHO, 7, 13, 14, 19, 39, 40, 42, 44, 45, 48, 49, 51,
USA, 35, 45, 47, 112 61, 68, 71, 72, 73, 74, 86, 87, 105, 134
UV, 111 workers, 63, 85
UV radiation, 111 working memory, 91
World Health Organisation, 7, 19, 105
World Health Organization (WHO), 34, 35, 36, 39,
V 42, 44, 49, 61, 90, 102, 104, 122, 134
worldwide, 45, 102
variables, 12, 36, 39, 54, 123, 132, 134 worry, 96
variations, 34, 73, 96, 110, 134
vegetables, 29, 51, 59, 109, 133
vehicles, 132 X
victimization, 85, 87
victims, 69, 85 xerostomia, 24
Vietnam, 62
viral pathogens, ix, 107, 108
viruses, 70, 74
Y
vitamin D, vii, x, 4, 23, 31, 40, 46, 49, 53, 56, 58, 59,
young adults, 64
60, 63, 65, 107, 108, 109, 110, 111, 112, 113,
young people, vii, 1, 2, 29, 30, 103
115, 116, 117, 118, 119
young women, 65
vitamin D deficiency, 40, 56, 63, 116
vitamin K, 4, 23, 31
vitamins, viii, 6, 22, 43, 45, 53, 96, 97, 116, 119 Z
VLDL, 10, 11
vomiting, vii, 1, 4, 5, 12, 15, 17, 18, 20, 22, 23, 24, zinc, 4, 10, 23, 28, 31, 47, 56, 57, 60, 62, 97
27, 30, 33

Child Nutrition and Health

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CHILDREN'S ISSUES, LAWS AND PROGRAMS

CHILD NUTRITION AND HEALTH

Additional books in this series can be found on Nova’s website

Additional E-books in this series can be found on Nova’s website

NUTRITION AND DIET

Additional books in this series can be found on Nova’s website

Additional E-books in this series can be found on Nova’s website

CHILD NUTRITION AND HEALTH

NOTICE TO THE READER

LIBRARY OF CONGRESS CATALOGING-IN-PUBLICATION DATA

Published by Nova Science Publishers, Inc.  New York

Nutrition in Children and Adolescents

Terezie Tolar Mosby1 and Ronald D. Barr2,

1. Nutritional Status at Diagnosis

Impact of Over and Undernutrition

II. Overnutrition (Overweight and Obesity)

2. Nutritional Status during Treatment

Table 1. Nutritional screening for nurses: inpatients done at admission; outpatients

Are you currently being seen by the clinical nutrition service?

2. Data Collection, Evaluation and Interpretation

In depth nutritional assessment should be provided anytime patients are at risk of

Nutrition-Focused Physical Examination

Anthropometry and Measures of Body Composition

Table 2. Calculation of body mass index (BMI)

II. Midlevel Measures

A. Estimated IBW in children and adolescents

B. Weight as a percentage of ideal body weight:

III. Advanced Measures

Biochemical and Hematological Indices

experience an increase in plasma total triacylglycerol concentration (a measure of fat stored in

II. Delayed Hypersensitivity Testing

III. Prognostic Nutritional Nutritional Index

IV. Creatinine Height Index

V. Maldigestion and Malabsorption

II. Dietary Intake

III. Comparison of Dietary Intake to Estimated Calorie Needs

Table 4. Nutritional risk

Weight for Age

 Less than the 5th or >85th percentile

Length or Height for Age

Weight for Length or Height

Body Mass Index (BMI)

 More than the 95th percentile - obese

Ideal Body Weight (IBW) calculated from weight for length/height

 More than110% - overweight

Ideal Body Weight (IBW) calculated from BMI

 More than120% - overweight

 More than the 95th percentile (may indicate macrocephaly)

Assessment of subcutaneous fat and muscle mass for signs of under/overweight

 Triceps skin fold estimation of energy stores - compare to reference values

Less than 50% of estimated energy needs for up to 3 days

C. Common Complications of Treatment

Protein Energy Malnutrition

PEM occurring in association with cancer is usually a mixture of inadequate intake

Cancer cachexia is a well recognized condition in which there is rapid deterioration in

GVHD is a potential complication following allogeneic HSCT. The donor's

systematic approach to management with a multidisciplinary team. Two means of treating

Veno-occlusive disease (VOD) is a potentially serious liver problem caused by high

Mucositis is a common occurrence in cancer patients. It is a painful inflammation and

Hemorrhagic cystitis is diffuse inflammation of the bladder leading to dysuria and

Table 5. Energy requirements (kcal) of pediatric HSCT patients

Age Calories (kcal)

Indirect calorimetry can be useful anytime hypermetabolism or hypometabolism is