Curr Obes Rep (2013) 2:10–22
DOI 10.1007/s13679-012-0042-7
ETIOLOGY OF OBESITY (JA MARTINEZ, SECTION EDITOR)
Multifactorial Influences of Childhood Obesity
Yeow Nyin Ang & Bee Suan Wee &
Bee Koon Poh & Mohd Noor Ismail
Published online: 30 December 2012
# Springer Science+Business Media New York 2012
Abstract Obesity is the result of complex interactions of
multiple factors that have gradually led to enduring
changes in lifestyles, and thus, creating a global epidemic
of major health concerns. The roles of genetics and the
environment are vital and need to be explored to further
our understanding of the etiology of childhood obesity.
This review critically looked at published reports over
the past decade on factors that are unmodifiable, such as
genetics, ethnic differences, gestational weight and intra-
uterine conditions; as well as modifiable factors, such as
socioeconomic status, diet, physical activity, sleep, and
parental determinants. With the worldwide increase in
prevalence of pediatric obesity over the past several
decades, it is imperative that we understand the root
causes of obesity in order to arrest the rising trend
through better prevention and intervention strategies.
Keywords Child . Obesity . Adiposity . Body composition .
Multifactorial influences
Y. N. Ang : B. S. Wee : B. K. Poh
Nutritional Sciences Program, School of Healthcare Sciences,
Faculty of Health Sciences, Universiti Kebangsaan Malaysia,
Kuala Lumpur, Malaysia
B. S. Wee
Faculty of Medicine and Health Sciences,
Universiti Sultan Zainal Abidin, Kuala Terengganu, Malaysia
M. N. Ismail (*)
Department of Nutrition and Dietetics, Faculty of Health Sciences,
MARA University of Technology, 42300,
Puncak Alam, Selangor, Malaysia
e-mail: ismail_noor@puncakalam.uitm.edu.my
M. N. Ismail
e-mail: ismailnoor49@gmail.com
Introduction
Childhood obesity is portrayed by the accrual of exces-
sive body fat as well as the growth of excess adipocytes
[1]. It is widely accepted as has been reported that
overweight or obese children are at greater risk of becoming
overweight or obese adults; who will face a life-time of
increased risk for various diseases, including diabetes melli-
tus, cardiovascular disease, liver disease and certain cancers
[2, 3]. Even during childhood, obesity has been reported to
increase the risk for various medical problems, such as
prediabetes and diabetes, metabolic syndrome, cardiovascu-
lar, pulmonary, orthopedic and gastrointestinal diseases, as
well as psychological problems [3–5].
The incidence of overweight and obesity has great
implications for public health. Globally, the prevalence
of overweight and obesity has increased at an alarming
rate. According to the World Health Organization (WHO),
it is estimated that more than 40 million children under
five years of age were overweight in year 2010, with
close to 35 million of these children in developing
countries [6]. Based on secular trends using the Interna-
tional Obesity Task Force (IOTF) criteria, Wang and
Lobstein [7] estimated overweight to occur in 46% of
school-aged children in the Americas, 41% in the Eastern
Mediterranean region, 38% in the European region, 27%
in the Western Pacific, and 22% in the Southeast Asia.
At the individual level, determinants of obesity include
genetics, biology, behavior, and environments that foster
an adverse balance between energy intake and energy
expenditure [8]. However, there are also other relevant
factors related to childhood obesity, including dietary
status, physical activity, sleep duration, socio-economic
status and intrauterine factors. It is therefore necessary
to further explore the causal factors that contribute to
obesity in children. Table 1 summarized the findings of
recent studies on childhood obesity, while Fig. 1 presents the
Curr Obes Rep (2013) 2:10–22 11

Table 1 Summary of recently reported studies on childhood obesity

Authors (year) Study design Participants Observations Main outcomes

Studies related to genetic factors

Speliotes Two-stage genome-wide 249,796 European Identified and validated BMI- A total of 32 BMI-associated loci
et al. (2010) association meta-analysis children and adults associated loci. were confirmed. These genes in-
[20••] creased the odds of overweight
by 1.013 to 1.138-fold and of
obesity by 1.016- to 1.203-fold.
Faith Twin study 69 same-sex twin pairs Genetics and environment Poorer compensation among
et al. (2012) aged 4-7 years, including influenced self-regulatory eat- African American and Hispanic
[27] 40 monozygotic and 29 ing and body fat of children. as compared to European
dizygotic pairs in the USA American children and lesser
self-regulatory eating was associ-
ated with greater body fat.
Li et al. (2009) Two generation birth 16,794 parents measured Increased parental BMI and Childhood BMI increased between
[133] cohort study several times from age 7 excessive parental BMI gains the two generations by 0.25-1.10
to 33 years and 2908 during childhood and unit; and the effect of parental
offsprings aged 4-18 years adulthood were associated BMI in childhood as well as that
in England, Scotland, with a higher BMI and higher in adulthood had similar effect on
and Wales obesity risk in their children. the BMI of their offspring
Studies related to ethnic factors
Liu et al. Cross-sectional study 1039 children aged 8-10 Ethnic differences in the Asian children had 3-6 units lower
(2011) [45] years (352 Chinese, 155 relationship between body BMI at a given percentage body fat
Lebanese, 197 Malay, 112 mass index and percentage compared to Caucasian children.
Filipino and 223 Thai) body fat among Asian children
from different background.
Lakshmi Cross-sectional study 262 white Caucasian Differences in body composition Asian Indian children had smaller
et al. (2012) children in UK and 626 and metabolic status between body mass index and waist
[43] Indian children in India. white UK and Asian circumference than Caucasian;
Indian children and both Indian boys and girls
had higher percent body fat.
Cuypers Prospective study 1450 adolescents from Association between cultural Protective influence of cultural
et al. (2012) Norwegian HUNT study and social activities were activities in female adolescents
[51] (1995-97) who were measured in young adulthood, against overweight in adulthood
followed up (2006-2008) interaction effect of a genetic and moderating effect on obesity
as young adults. predisposition score by leisure susceptibility genes.
time activities were tested.
Studies related to gestational weight and intrauterine factors
Ferraro Two generation birth 4321 mothers aged 16-50 High maternal pre-pregnancy Overweight or obese mothers who
et al. (2012) cohort study years and their infants in BMI and excessive gestational exceeded the GWG
[56•] Ottawa and Kingston weight gain (GWG) increases recommendations had higher
the risk of giving birth to chances of delivering a large baby
a large-for-gestational by 3-folds (OR03.59) and 6-folds
age infant. (OR06.71) compared to normal
weight mothers
Studies related to socio-economic factors
Moraeus Cross sectional study 3636 children in Sweden Urbanization level and parental Boys had greater risk of obesity in
et al. (2012) characteristics, such as weight semi-urban and rural areas but
[72] status and education, are this was not true for girls.
related to risk of overweight
in children
Studies related to dietary factors
Disantis Retrospective study 109 children aged 3- 6 years Behavioural mechanisms Children who were directly
et al. (2011) in US contributed to the relationship breastfed had greater appetite
[83] between breastfeeding and regulation compared with
lower obesity risk. children fed human milk in a
bottle. Directly breastfed children
were more likely to have high
satiety responsiveness.
12 Curr Obes Rep (2013) 2:10–22

Table 1 (continued)

Authors (year) Study design Participants Observations Main outcomes

Eloranta Cross-sectional study 510 children aged 6-8 years Dietary factors are associated Having all three main meals, satiety
et al. (2012) in Kuopio, Finland. with overweight (OW), per- responsiveness and slowness in
[89] cent body fat (%BF), waist eating were inversely associated
circumference (WC) and hip with OW, %BF, WC and HC. On
circumference (HC) the other hand, enjoyment of
food, food responsiveness,
emotional overeating and protein
intake were directly associated
with OW, %BF, WC and HC.
Antonogeorgos Cross-sectional study 700 children aged 10-12 Consumption of breakfast Synergistic effect of consuming
et al. (2011) years old in Athens and frequent meal lower more than three meals and
[90] obesity risk. breakfast everyday were two
times less likely to be overweight
or obese (OR0 0.49).
Studies related to physical activity factors
Özmert Cross-sectional study 860 children aged 12-15 Positive correlation between Children with a BMI z-score
et al. (2011) years in Turkey television viewing and other above 2SD watched television
[113] sedentary activities, such as (2.5±0.9h/day) longer than those
reading, watching CD and with BMI z-score below -2SD
computer use. (1.6±0.8h/day).
Metcalf Prospective cohort study 202 children in England Physical inactivity appears to be %BF was predictive of changes in
et al. (2011) the result of fatness rather than PA over the following 3 years,
[116] its cause. but PA levels were not predictive
of subsequent changes in %BF
over the same follow up period.
Studies related to sleep factors
Carter 3-year longitudinal cohort 244 children aged 3-7 years Reduced sleep duration Each extra hour of sleep at ages 3-5
et al. (2011) observational study in New Zealand increased BMI and body fat years was associated with 2 times
[128•] in children. lower BMI (OR00.48), reduced
overweight risk (OR00.39) and
fat mass index (OR00.43) at age
7 years.
Studies related to parental determinants factors
Morrissey Cross-sectional study 990 children aged 8-12 Mothers’ employment was Every period of 5.3 months of
et al. (2011) years in 10 cities associated with increases in mother’s employment increased
[132] children’s BMI, especially in child’s BMI by 10% of a standard
older children. deviation. Moreover, maternal
employment also increased
likelihood overweight risk by
6 times among children in
sixth grade.

conceptual framework identifying several major modifiable
and unmodifiable risk factors that may exert substantial influ-
ence on the etiology of childhood obesity.
Unmodifiable Risk Factors in Childhood Obesity
Genetic Influences
Genetic susceptibility to obesity is recognized as a highly
heritable condition that begins at an early age. Genetic
factors also determine whether one is susceptible to other
obesity-related diseases [9]. Monogenic obesities have been
examined extensively in children given that these conditions
are rare, very severe, and generally begin in childhood.
Candidate gene approaches have been used to identify the
association between a variant or mutation within or near the
candidate gene and a trait of interest (for example: obesity).
With respect to single-gene mutation, a number of genes
have been identified in individuals who were severely
obese, namely pro-opiomelanocortin (POMC), proprotein
convertase subtilisin/kexin 1 (PCSK1), melanocortin-4
receptors (MC4R), corticotrophin-releasing hormone recep-
tor (CRHR), leptin (LEP), leptin receptor (LEPR), cocaine-
and amphetamine-regulated transcript (CART), brain-
derived neurotrophic factor (BDNF) and single-minded ho-
molog 1 (SIM-1) [10–16]. The defects in POMC produced
altered peptide which is different from α-melanocyte-
Curr Obes Rep (2013) 2:10–22
Fig. 1 Conceptual framework
describing the etiology of
childhood obesity
stimulating hormone (α-MSH) through PCSK1 and without
α-MSH, MC4R is unable to play a role in weight regulation
[10]. Deficiency of MC4R was found to associate with
obesity by accelerated linear growth and increased final
height as well as excess in insulin and partially suppress
growth hormone [11]. Meanwhile, CRHR shows anorexi-
genic hypothalamic response by activation of urocortin to
potently suppress food intake [12]. LEP and LEPR suppress
the increase of CART [13] and prevent overeating by con-
trolling the appetite [14]. BDNF have been implicated in the
energy regulation by increasing gene expression for LEPR
and POMC [15]. SIM1 are key factors interacting with the
central melanocortin pathway in the control of appetite by
decreasing MC4R [16]. However, cases of single-gene obe-
sity cannot explain many others with latent genetic predis-
position that is expressed only upon exposure to an
obesogenic environment.
In most individuals, obesity results from the interac-
tion of multiple genes that encode peptides that transmit
hunger and satiety signals, regulate adipocyte growth
and differentiation and control energy expenditure [17].
The Human Obesity Gene Map reported 253 loci from
61 genome-wide linkage scans, of which 15 loci have
been replicated in at least three studies [18]. However, a
meta-analysis by Saunders et al. showed that genome-
wide linkage analysis may not be the best method for
identifying genetic variants for obesity [19].
13
Genome-wide association studies (GWAS) have impli-
cated many genetic loci for obesity in the past 5 years
[20••], and of particular interest, the fat mass and
obesity-associated protein (FTO) gene [21]. FTO gene
expression in the hypothalamic arcuate nucleus was de-
termined to contribute significantly to obesity as a con-
sequence of hyperphagia, seemingly in the absence of
changes in energy expenditure [22, 23]. Two other genes,
TNNI3K and POMC, were identified by GWAS as being
associated with childhood obesity [24]. In 2010, a study
discovered two additional obesity loci (TNKS-MSRA and
SDCCAG8) in extremely obese children and adolescents,
with odds ratios of approximately 1.10 per risk allele for
both loci for early-onset obesity [25].
Furthermore, gene-environment interactions also play
an important role in childhood obesity [26, 27]. Differ-
ences in body composition is also a likely factor; specif-
ically the lower abdominal adiposity found in African-
American children compared with European or Hispanic
American children [28, 29], and the higher trunk skinfold
thickness in Chinese girls compared to Malaysian and
Lebanese girls [30]. These differences in body composi-
tion phenotype suggest that the genetic makeup of indi-
viduals interacts with environmental factors from early
developmental stages, as has been demonstrated by Fer-
nandez et al. [26] and the twin and adoption study [31].
With the advent of next-generation sequencing techniques
14
and advances in the field of exposomics, sensitive and
specific tools to predict the obesity risk as early as possi-
ble are the challenges in the coming decade [32].
An environmental factor of major importance is nutrition.
The risk of obesity is higher when an individual with a high-
risk genetic profile is exposed to high-risk environment. For
example, the Pima Indians have an inherent susceptibility to
obesity, and obesity is more likely to develop among those
living in Arizona as they are exposed to obesity-promoting
environments, such as ‘Western diet’ and less exercise, com-
pared with Pima Indians living in Mexico, who survive on
traditional food and manual labor [33]. Moreover, obesity
genes might also play a role in the choice and preference of
dietary intake of saturated fat, carbohydrates, mono- and dis-
accharides, and polysaccharides [34]. A longitudinal study
had suggested that high consumption of saturated fat increase
the obesity risk associated with FTO gene [35]. To date, the
genes responsible for individual differences in sensitivity to
changes in energy balance have not all been identified. In view
of the complexity of the biological systems involved in body
weight regulation, these genes are likely to be numerous [36].
Di Castelnuovo et al. [37] suggested that positive assor-
tative mating by BMI may assemble obesity-promoting risk
alleles and probably undergo interaction between gene and
environment in a family [38]. A recent paper revealed that
weight changes over a period of two years was associated
with marital status; partly due to shared environment, such
as the stimulus to eat when dining together or the motivation
for weight control to increase attractiveness [39]. Compar-
ing children born to normal weight parent, children had
higher obesity risk if they had an obese father
(OR02.11), an obese mother (OR07.66), or two obese
parents (OR08.05) [40]. These observations suggested
that assortative mating is related to the epidemic of
childhood obesity.
Ethnic Differences
Ethnic disparities have been widely discussed as a con-
tributing factor to adiposity. In adults, very large differ-
ences between ethnic groups, especially among women,
have been observed, with non-Hispanic black individu-
als exhibiting the highest prevalence of obesity [41].
Asian Indian individuals were observed to have signif-
icantly greater total abdominal fat and intra-abdominal
adipose tissue and truncal subcutaneous (SC) adipose
tissue than Caucasians [42]. Similarly in children, South
Asian Indians reportedly had smaller body mass index
and waist circumference than Caucasians, and yet both
boys and girls from India had higher percent body fat
[43]. Hispanic Americans exhibit the greatest trunk,
intra-abdominal and SC adipose tissue, followed by
European Americans and African American [44•].
Curr Obes Rep (2013) 2:10–22
In comparison with Caucasian children of the same age,
Asian children have lower BMIs by 3-6 units for a given
percentage of body fat [45]. Ethnic differences in adipos-
ity had been reported in adolescence, with greater central
adiposity being observed in women of Asian ancestry
compared with Caucasians [46]. For a given BMI, chil-
dren and infants of South Asian origin have higher
adiposity compared with White Europeans, suggesting
that either genetic factors or exposure to maternal phys-
iology contribute to obesity rather than behaviors or diet
during childhood or later in life [47].
The risk factors for obesity reportedly exist from as early
as the prenatal and early childhood periods [48]. Taveras et
al. [49] further suggested that racial or ethnic differences in
childhood obesity may be determined by several factors that
operate during pregnancy, infancy and early childhood.
Compared to Caucasian children, children of Black and
Hispanic ancestry had higher odds of rapid infant weight
gain, and exhibited lower birth weights for gestational age
but had higher BMI z-scores, and a greater prevalence of
obesity at the age of three years [49].
Amongst ethnic groups, cultural differences are be-
lieved to be one of the contributing factors to the dis-
parities in childhood obesity [50]. For instance,
perception on body image occurs in a cultural context
and differs by ethnic groups. Women who traditionally
feed, educate and take care of their children, also possess
their own beliefs about body image, which in turn will
have implications toward their children’s own body im-
age [50]. In addition, cultural activities may also be
considered as a non-modifiable factor in determining a
child’s adiposity. A recent prospective study [51] found
negative association between participation in cultural ac-
tivities with z-scores of waist circumference (WC) and
waist-to-height ratio (WHR) in girls; and concluded that
cultural activities had a moderating effect on the obesity-
susceptibility genes. Although environmental factors per-
taining to health-related behaviors or lifestyles and eco-
nomic disadvantage could contribute to some of the
ethnic differences in the prevalence of diseases associat-
ed with obesity, these factors cannot explain all the
differences in expression and disease patterns due to race
or ethnicity. Hence, it is likely that genetics or molecular
factors also contribute to the racial disparities in obesity-
related comorbidities [52].
Gestational Weight and Intrauterine Factors
The intrauterine environment plays a crucial role in the
development of obesity, type 2 diabetes mellitus and meta-
bolic syndrome in the offspring [53, 54]. Shankar and col-
leagues [55] illustrated that children exposed to maternal
obesity in utero were more susceptible to obesity, regardless
Curr Obes Rep (2013) 2:10–22
of birth weight, which seems to indicate that subtle
programming of obesity occurs in the absence of clear
changes in birth weight. Children of overweight or obese
mothers also had more likelihood of being born large for
gestational age (LGA) [56•]. These children are at an in-
creased risk of obesity when they also exhibit a high birth
weight of more than 4 kg [57].
Pre-pregnancy obesity is the strongest risk factor for
childhood obesity [58] and metabolic dysregulation [59].
Higher gestational weight gain (GWG) has been associ-
ated with both a greater incidence of pre-eclampsia [60]
and a significantly higher risk of gestational diabetes
mellitus (GDM) with maternal hyperglycemia as well as
fetal hyperglycemia, which can consequently lead to ex-
cess fetal insulin and thus fetal overgrowth [61]. Hull
and colleagues demonstrated direct relationship between
weight gain during pregnancy and birth weight or infant
adiposity [62]. Longitudinal data have revealed a strong
relationship between gestational weight gain and child-
hood weight status, regardless of the mother’s pre-
pregnancy weight [63] and also independent of genetic
factors [64]. It has been suggested that weight status
during early human development, especially in the ma-
ternally overweight or obese children, can have on-going
effects on adiposity and related chronic diseases [65].
In the in utero environment, epigenetic factors may alter
gene expression and predispose the fetus to abnormal phys-
ical activity and dietary behaviors later in life by compro-
mising the physiological thresholds for energy balance
regulation [66]. Moreover, the offspring’s susceptibility to
premature chronic diseases may be influenced by constant
exposure to excess energy, hormones and growth factors in
utero [54]. Human data regarding the effect of maternal
lifestyle on epigenetic modifications are scarce; however,
animal-model research has demonstrated that the body com-
position of the offspring changes with maternal diet and is
associated with epigenetic alterations in metabolic control
genes [67]. Furthermore, the maternal diet may influence the
food preferences and feeding responses in the offspring
[68]; and, if nutritionally compromised, may promote adi-
posity as well as early onset of metabolic impairments in the
child [69]. The intake of glucose and lipids, such as trigly-
cerides and non-esterified fatty acids, had also been shown
to have positive relationship with fetal growth [70, 71•].
Modifiable Risk Factors of Childhood Obesity
Socio-economic Status (SES)
Living conditions and societal factors have great impact on a
child’s weight status. In Sweden, boys living in semi-urban
and rural areas have a greater risk of obesity [72]. In many
15
developed countries, lower socioeconomic groups reported-
ly had the highest levels of overweight and the lowest levels
of physical fitness, and adolescent girls were particularly at
risk [73]. In most countries, children in urban areas were
more likely to be obese than those in rural areas. Contem-
porary populations of children were found to exhibit higher
rates of obesity than do those from the lowest socioeconom-
ic groups in high-income countries [74]. In India, signifi-
cantly more children of higher SES status were obese and
overweight than those from lower SES [75, 76].
Positive energy balance, high energy intake, and low
levels of energy expenditure on physical activity are
strongly associated with urbanization and economic afflu-
ence [77]. SES groups, usually low-SES in industrialized
countries and high-SES in developing countries, with
greater access to energy-dense diets are at a higher risk
of being obese. However, the obesity–SES association
varies with gender, age, and country [78••]. The findings
from a longitudinal survey suggest that rather than hav-
ing a major direct causative role, family income may act
primarily as a proxy for other unobserved characteristics
that determine children’s weight status [79].
Diet
Breast-feeding is known to have a consistent protective
effect against obesity in children [80]; however, a quantita-
tive review by Owen et al. concluded that the precise mag-
nitude of association is still unclear [81]. The macronutrient
composition and bioactive substances of breast milk may
influence metabolic programming and the regulation of
body fatness and growth rate [80]. Formula-fed infants had
higher insulin levels and lower leptin levels compared with
breast-fed infants; and these proteins could stimulate fat
deposition and lead to the early development of adipocytes
[82]. Direct breastfeeding during early infancy has been
related to better appetite regulation later in childhood;
whereby a study showed that children who were fed human
milk in a bottle during the first three months of life were
67% less likely to have good response to satiety during their
preschool years compared to children who were directly
breastfed [83]. The effect of breastfeeding on infant growth
may be a significant determinant of early life programming
for obesity and chronic diseases later in life, especially for
the offsprings of women with diabetes [84].
The adoption of industrialized Western society lifestyles,
including urbanization, Western foods, increased sedentari-
ness and car ownership, has been related to increased obe-
sity. Rapid and marked socio-economic advancement has
brought about considerable changes to the lifestyles of com-
munities, including among children; especially with respect
to dietary patterns, such as the high intake of energy-dense
food, which has been identified as an important factor in
16
body weight control in adults, as well as in children and
adolescents [85]. Moreover, alterations in meal patterns
are also evident with more families eating out, skipping
meals especially breakfast and relying too much on fast
foods, which are known to be high in saturated and trans
fats, energy dense, and served in large portion sizes
[86–88]. Children who ate all three main meals, namely,
breakfast, lunch and dinner, daily were reported to have
63% lower risk of being overweight or obese than those
who did not [89]. Another study had also further con-
firmed the protective role of consuming three meals per
day with a lower likelihood of overweight or obesity, but
only if breakfast was not skipped [90]. Skipping break-
fast has been shown to affect children's appetite but not
their energy intake at subsequent meals [91•]. When
children did not consume breakfast, they were hungrier,
less full, and could consume more food prior to lunch;
hence, increasing daily dietary intake [92].
The rapid development of fast-food outlets and the
easy availability of junk food is also a matter of concern.
Children with working parents who are cared for by care
providers are more likely to receive food that is high in
energy and of poor nutritional value, perhaps because
care providers are more concerned with placating their
wards than with the long-term health of the children [93].
Furthermore, parents who work outside of the home may
also serve more high-calorie pre-prepared, convenience,
or fast foods due to time constraints. Additionally, unsu-
pervised children tended to make poorer nutritional
choices when preparing their own snacks [94]. It has
also been reported that children consumed more fast food
items and carbonated drinks as compared to fruits and
vegetables, as these food items were easily available
through vending machines and school canteens [91•].
Changes in lifestyle, dietary habits, and food marketing
have brought about undesirable effects, with large propor-
tions of the population afflicted with various non-
communicable diseases associated with over-nutrition, in-
cluding obesity [95–97]. Available evidence suggests that
high-energy intake in early infancy and high consumption of
energy-dense foods and sweetened drinks during childhood
is associated with increased adiposity [85].
Food marketing to children has been proposed as a means
for addressing the global crisis of childhood obesity in
recent years. The commercial advertising and marketing of
food and beverages influences the diet and health of chil-
dren and youths. An estimated more than $10 billion a year
is spent on marketing of all types of food and beverages to
children and youths in America [98]. There is evidence that
food marketing to children is (a) massive; (b) expanding in
number of avenues, such as product placements, video
games, the internet, and cell phones; (c) composed of mes-
sages that are almost entirely for nutrient-poor, calorie-dense
Curr Obes Rep (2013) 2:10–22
foods; (d) having harmful effects; and (e) increasing glob-
ally and thus difficult to regulate by individual countries
[99]. Recently, WHO has produced a set of recommenda-
tions to help member countries to either develop or strength-
en policy related to marketing of foods and non-alcoholic
beverages to children [100].
More recently, vitamin D deficiency has been identified
as a new global public health issue. Vitamin D has been
suggested to be a potential factor in the prevention of many
illnesses, including obesity [101]. Obese individuals were
observed to have lower concentrations of 25-hydroxy vita-
min D, suggesting that obese individuals may have altered
vitamin D and parathyroid hormone physiology [102].
Physical Activity
Physical activity has long been recognized as one of the
important determinants of obesity [103] and as a promoter
of lifelong positive health behavior in children [104]. The
importance of physical activity lies in the basic concept of
the Law of Thermodynamics, from which can be derived the
fact that human energy expenditure consists of three com-
ponents; namely, energy that is expended for thermogenesis,
energy that is expended for basal metabolism or the basal
metabolic rate, and energy that is expended on physical
activity [105]. Of these, physical activity is the only factor
that can be modified to prevent obesity.
It has been reported that only a third of overweight and
obese children engaged in a minimum of 60 minutes of
physical activity daily, which suggests that the younger
generation led sedentary lifestyles [106]. School children,
especially those in Asian countries, have been reported to
focus more on academics and are less involved in sports and
physical activities [107]. Children also spent much of their
leisure time engaged in sedentary activities, such as watch-
ing TV or playing computer/video games [108]. Studies
have found that normal BMI values were distributed in the
higher tertiles of physical activity [109, 110].
A systematic review by Te Velde et al. [111] con-
firmed that there is an inverse association between total
physical activity and overweight; but not, with respect
to specific sub-behaviors, such as moderate to vigorous
physical activity, aerobic exercise and leisure activity.
Jimenez-Pavon et al. also presented evidence that sup-
ports negative association between objectively measured
physical activity and adiposity, and reported that higher
levels of habitual physical activity are protective against
child and adolescent obesity [112].
Watching television decreases the amount of time
spent on active physical activities [113], and has been
associated with increased food consumption either during
television viewing or as an indirect result of food adver-
tisements [114]. A study involving students aged 11 to
Curr Obes Rep (2013) 2:10–22
13 years in California concluded that time spent watching
television was significantly associated with obesity [113].
Te Velde et al. [111] also reported moderate evidence for
a significant positive association between TV/video/com-
puter screen time and overweight. Increased physical
activity and decreased screen-based sedentary behavior
were associated with decreased body fat percentages but
not decreased BMI [115].
Although the benefits of physical activity have been
proven in many studies [103, 104, 111–113], there are a
few studies that reported contradicting results regarding
physical activity and obesity. A longitudinal study in
England found that physical inactivity is the result rather
than the cause of obesity, and argued that inactivity does
not lead to fatness; hence, explaining why physical ac-
tivity interventions sometimes fail to prevent excess
weight gain in children [116]. Another intervention pro-
gram conducted among preschool children, reported that
physical activity helped to improve motor skills but
failed to reduce body mass index [117].
Sleep
Sleep plays an important role in the health of children
and adolescents as it allows for the normal diurnal
rhythm of hormones that are related to growth, matura-
tion, and energy homeostasis [118•]. Children who sleep
for shorter durations have been postulated to have lower
energy intake and expenditure; since sleep deprivation is
known to lead to alterations in the structure of sleep
stage, and hence, giving rise to fatigue, daytime sleep-
iness, somatic and cognitive problems and low activity
levels [119]. Several studies have reported that habitual
sleep length is prospectively and independently associ-
ated with obesity and mortality [120, 121] with those
who sleep for short durations being more likely to be
obese [122]. On the other hand, longer sleep duration
may reduce the opportunity to eat, and thus prevent
over-eating among children and adolescents [123].
Sleep deprivation influences the development of obe-
sity through several possible biological pathways. These
include increased sympathetic activity, decreased leptin
and growth hormone, elevated cortisol and ghrelin lev-
els, and impaired glucose tolerance [124]. Hormonal
alterations may contribute to the selection of energy-
dense food, excessive energy intake, changes in energy
expenditure, insulin resistance, alterations in the basal
metabolic rate, modifications in the thermic effect of
food and non-exercise activity thermogenesis [123,
125]. As short sleep duration has been clearly associat-
ed with increased risk of childhood obesity, sleep could
be a vital factor that needs to be considered in child-
hood obesity prevention [125].
17
Visceral adiposity is a significant predictor of obstructive
sleep apnea (OSA), with the severity being independent of
BMI among obese children [126]. This is supported by
another study in which obese children exhibited no difference
in head, neck and abdominal subcutaneous fat but instead
exhibited more abdominal visceral fat [127]. A longitudinal
study revealed that children who slept less were more likely to
be overweight and had high body fat values [128•]. Besides,
sleep duration decreases with age whereas higher body fat
mass and BMI both tend to increase with age [129].
Based on a meta-analysis, the recommended sleep dura-
tions are 11 hours or more for children aged below 5
years, 10 hours or more for children aged between 5
and 10 years, and 9 hours or more for children aged 10
years and above [125]. Independent of other risk factors,
increasing sleep duration may decrease the prevalence of
childhood obesity [130]. The current available evidence is
unable to support claims of a secular trend [131]. Future
randomized intervention trials are necessary to determine
the effectiveness of sleep extension for the prevention of
obesity among children and adolescents [130].
Parental Determinants
Parental work schedule [132], parental BMI [133], and
maternal smoking habits [134] appear to be important in
determining children’s health status, particularly with re-
spect to a healthy body weight. Maternal smoking during
pregnancy may be a risk factor for childhood obesity,
along with low birth weight [135]. A possible explanation
for this may be the impact of catch-up growth in the first
year of life on childhood obesity [136]. Children whose
mothers smoked during pregnancy were at increased risk
for overweight at the ages of 3 to 33 years [134]. Al-
though the mechanisms by which maternal smoking influ-
ences the weight of the child are not well characterized,
they are possibly due to nicotine, which is transported
across the placenta, and carbon monoxide, which poten-
tially influences placental vascular function and may cause
fetal hypoxia [134]. Nicotine acts to reduce appetite [137]
and body weight, while withdrawal results in hyperphagia
and weight gain [138]. It has been suggested that the
rapid weight gain of the infant during the early postnatal
period may be due to the effect of nicotine withdrawal,
similar to the increased craving for food [139].
A positive association has also been observed between
childhood obesity and parental BMI. Excessive gains in
parental BMI during youth and later life were found to
be associated with higher BMI and risk of obesity in the
offspring [133]. Similarly, child overweight/obesity was
also significantly associated with maternal work hours
and paternal non-standard work schedules [132, 140].
However, further research is required to determine the
18
manner in which non-standard work schedules disrupt
family life, the quality of children’s diet and their oppor-
tunity to participate in physical activity [141].
Conclusion
Obesity is considered to be an epidemic given that its
prevalence and severity in both adults and children is
rising at alarming rates. This increase is related to the
interactions between genetic makeup, intrauterine fac-
tors, and environmental living conditions. Obesity may
result from genetic susceptibility to a single gene or due
to the interactions of multiple genes that influence ap-
petite regulation, adipocyte growth and energy expendi-
ture. Ethnic disparities also contribute to childhood
adiposity. Moreover, children from low socioeconomic
families in industrialized countries and high socioeco-
nomic background in developing countries are at a
higher risk of being obese due to easy accessibility of
energy-dense food. Maternal weight status prior to or
during gestation may also be a key factor related to the
short- and long-term risks of childhood obesity. Further-
more, other parental determinants, such as maternal
smoking and lengthy work duration, may worsen the
risks of childhood obesity. Contemporary lifestyle
changes are also important influences leading to child-
hood obesity; these changes include increasingly seden-
tary activities, unhealthy dietary habits and lower
quality of sleep. Therefore, deeper understanding of
the multi-factorial contributors to obesity is of utmost
importance in order to aid in the development of effec-
tive interventions aimed at reducing the rates of occur-
rence of global obesity.
Disclosure No potential conflicts of interest relevant to this article
were reported.
References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major importance
1. Helba M, Binkovitz LA. Pediatric body composition analysis
with dual energy X-ray absorptiometry. Pediatr Radiol. 2009;39
(7):647–56.
2. International Food Information Council Foundation: Moving to
prevent childhood obesity. Available at www.foodinsight.org/
Newsletter/Detail.aspx?topic0Moving_to_Prevent_Childhood_
Obesity. Accessed October 2012.
Curr Obes Rep (2013) 2:10–22
3. Gahagan S. Child and adolescent obesity. Current Problems in
Pediatric and Adolescent Health Care. 2004;34:6–43.
4. Quah YV, Poh BK, Ismail MN. Metabolic syndrome based on
IDF criteria in a sample of normal weight and obese school
children. Malaysian J Nutr. 2010;16(2):207–17.
5. Wee BS, Poh BK, Bulgiba A, et al. Risk of metabolic syndrome
among children living in metropolitan Kuala Lumpur: a case
control study. BMC Publ Health. 2011;11:333.
6. World Health Organization: Global strategy on diet, physical
activity and health: Childhood overweight and obesity.
Available at http://www.who.int/dietphysical activity/children/
en/. Accessed October 2012.
7. Wang Y, Lobstein T. World wide trend in childhood overweight
and obesity. Int J Pediatr Obes. 2006;1:11–25.
8. Budd GM, Hayman LL, Faan RN. Childhood obesity, determi-
nants, prevention and treatment. J Cardiovas Nurs. 2006;21
(6):437–41.
9. Anderson PM, Butcher KF, Levine PB. Economic perspectives
on childhood obesity. Econ Perspectives. 2003;27(3):30–48.
10. Mountjoy K. Functions for pro-opiomelanocortin-derived
peptides in obesity and diabetes. Biochem J. 2010;428:305–
24.
11. Martinelli CE, Keogh JM, Greenfield JR, et al. Obesity due to
melanocortin 4 receptor (MC4R) deficiency is associated with
increased linear growth and final height, fasting hyperinsuline-
mia, and incompletely suppressed growth hormone secretion. J
Clin Endocrinol Metab. 2011;96(1):E181–8.
12. Hsuchou H, Kastin AJ, Wu X, et al. Corticotropin-releasing
hormone receptor-1 in cerebral microvessels changes during de-
velopment and influences urocortin transport across the blood-
brain barrier. Endocrinology. 2010;151(3):1221–7.
13. Leshan RL, Opland DM, Louis GW, et al. Ventral tegmental area
leptin receptor neurons specifically project to and regulate
cocaine-and amphetamine-regulated transcript neurons of the ex-
tended central amygdala. J Neurosci. 2010;30(16):5713–23.
14. Davis JF, Choi DL, Schurdak JD, et al. Leptin regulates energy
balance and motivation through action at distinct neural circuits.
Biol Psychiat. 2011;69(7):668–74.
15. Byerly MS, Simon J, Lebihan-Duval E, et al. Effects of BDNF,
T3, and corticosterone on expression of the hypothalamic obesity
gene network in vivo and in vitro. Am J Physiol-Reg, I. 2009;296
(4):R1180–9.
16. Tolson KP, Gemelli T, Gautron L, et al. Postnatal Sim1 deficiency
causes hyperphagic obesity and reduced Mc4r and oxytocin
expression. J Neurosci. 2010;30(10):3803–12.
17. Farooqi IS. Genetic, molecular and physiological insights into
human obesity. Eur J Clin Invest. 2011;41(4):451–5.
18. Rankinen T, Bray MS, Hagberg JM, et al. The human gene
map for performance and health-related fitness phenotypes:
the 2005 update. Med Sci Sports Exercise. 2006;38
(11):1863–88.
19. Saunders CL, Chiodini BD, Sham P, et al. Meta-Analysis of
Genome-wide Linkage Studies in BMI and Obesity. Obesity.
2012;15(9):2263–75.
20. •• Speliotes EK, Willer CJ, Berndt SI, et al. Association analyses
of 249,796 individuals reveal 18 new loci associated with body
mass index. Nat Genet. 2010;42(11):937–48. This paper contin-
ued to identify the BMI-associated loci, which consisted of 14
known loci from previous GWA studies with additional 18 loci
from large Europe children. The authors were also examined the
association of the BMI loci with metabolic traits and the possible
function in body weight regulation.
21. Frayling TM, Timpson NJ, Weedon MN, et al. A common variant
in the FTO gene is associated with body mass index and predis-
poses to childhood and adult obesity. Science. 2007;316
(5826):889–94.
Curr Obes Rep (2013) 2:10–22
22. Wardle J, Carnell S, Haworth CM, et al. Obesity associated
genetic variation in FTO is associated with diminished satiety. J
Clin Endocrinol Metab. 2008;93(9):3640–3.
23. Speakman JR. A nonadaptive scenario explaining the genetic
predisposition to obesity: the “predation release” hypothesis.
Cell Metabolism. 2007;6(1):5–12.
24. Bradfield JP, Taal HR, Timpson NJ, et al. A genome-wide asso-
ciation meta-analysis identifies new childhood obesity loci. Nat
Genet. 2012;44(5):526–31.
25. Scherag A, Dina C, Hinney A, et al. Two new Loci for body-
weight regulation identified in a joint analysis of genome-wide
association studies for early-onset extreme obesity in French and
German study groups. PLoS Genet. 2010;6(4):e1000916.
26. Fernandez JR, Klimentidis YC, Dulin-Keita A, Casazza K. Genetic
influences in childhood obesity: recent progress and recommenda-
tions for experimental designs. Int J Obes. 2012;36:479–84.
27. Faith MS, Pietrobelli A, Heo M, et al. A twin study of self-
regulatory eating in early childhood: estimates of genetic and
environement influences, and measurement considerations. Int J
Obes. 2012;36:931–7.
28. Agfhani A, Goran MI. Racial differerences in the associatin of
subcutaneous and visceral fat on bone mineral content in prepu-
bertal children. Calcif Tissue Int. 2006;79:383–8.
29. Lee S, Kuk JL, Hannon TS, Arslaian SA. Race and gender
differences in the relationships between anthropometrics and
abdominal fat in youth. Obesity. 2008;16:1066–71.
30. Liu A, Byrne NM, Kagawa M, et al. Ethnic differences in body
fat distribution among Asian pre-pubertal children: a cross-
sectional multicenter study. BMC Publ Health. 2011;11:500.
31. Silventoinen K, Rokholm B, Kaprio J, Sørensen TIA. The genetic
and environmental influences on childhood obesity: a systematic
review of twin and adoption studies. Int J Obes. 2010;34:29–40.
32. Manco M, Dallapiccola B. Genetics of Pediatric Obesity.
Pediatrics. 2012;130(1):123–33.
33. Burrage LC, McCandless SE. Genetics of childhood obesity. US
Pediatrics Rev. 2007;1:60–3.
34. Bauer F, Elbers CC, Adan RA, et al. Obesity genes identified in
genome-wide association studies are associated with adiposity
measures and potentially with nutrient-specific food preference.
Am J Clin Nutr. 2009;90(4):951–9.
35. Phillips CM, Kesse-Guyot E, McManus R, et al. High Dietary
Saturated Fat Intake Accentuates Obesity Risk Associated with
the Fat Mass and Obesity–Associated Gene in Adults. J Nutr.
2012;142(5):824–31.
36. Bouchard C. Childhood obesity: are genetic differences in-
volved? Am J Clin Nutr. 2009;85(5):1494s–501.
37. Di Castelnuovo A, Quacquaruccio G, Donati MB, et al. Spousal
concordance for major coronary risk factors: a systematic review
and meta-analysis. Am J Epidemiol. 2009;169(1):1–8.
38. Power C, Pouliou T, Li L, et al. Parental and offspring adiposity
associations: insights from the 1958 British birth cohort. Annal
Hum Biol. 2011;38(4):390–9.
39. Jeffery RW, Rick AM. Cross-Sectional and Longitudinal
Associations between Body Mass Index and Marriage-Related
Factors. Obesity Res. 2012;10(8):809–15.
40. Ochoa MC, Azcona C, Moreno-Aliaga MJ, et al. Influence of
parental body mass index on offspring body mass index in a
Spanish population. Revista Espanola de Obesidad. 2009;7
(6):395–401.
41. Wang Y, Beydoun MA. The obesity epidemic in the United
States–gender, age, socioeconomic, racial/ethnic, and geographic
characteristics: a systematic review and meta-regression analysis.
Epidemiol Rev. 2007;29:6–28.
42. Misra A, Khurana L. Obesity-related non-communicable dis-
eases: South Asians vs White Caucasians. Int JObes. 2010;35
(2):167–87.
19
43. Lakshmi S, Metcalf B, Joglekar C, et al. Differences in body
composition and metabolic status between white UK and Asian
Indian children (EarlyBird 24 and the Pune Maternal Nutrition
Study). Ped Obes. 2012;7:347–54.
44. • Casazza KL, Hanks J, Beasley TM, et al. Beyond thriftiness:
independent and interactive effects of genetic and dietary factors
on variations in fat deposition and distribution across populations.
Am J Phys Anthropol. 2011;145(2):181–91. This paper described
the interactive contribution of genetic and diet in body fat storage
of children from different population. For instance, adiposity
measures were associated with European, particularly boys com-
pare to African and girls at their counterparts.
45. Liu A, Byrne NM, Kagawa M, et al. Ethnic differences in the
relationship between body mass index and percentage body fat
among Asian children from different background. Brit J Nutr.
2011;106:1390–7.
46. Morimoto Y, Maskarinec G, Conroy SM, et al. Asian ethnicity is
associated with a higher trunk/peripheral fat ratio in women and
adolescent girls. J Epidemiol. 2012;22(2):130–5.
47. Stanfield KM, Wells JC, Fewtrell MS, et al. Differences in body
composition between infants of South Asian and European an-
cestry: the London Mother and Baby Study. Int J Epidemiol.
2012;41(5):1409–18.
48. Reilly JJ, Armstrong J, Dorosty AR, et al. Early life risk factors for
obesity in childhood: cohort study. BMJ. 2005;330(7504):1357.
49. Taveras EM, Gillman MW, Kleinman K, et al. Racial/ethnic
differences in early-life risk factors for childhood obesity.
Pediatrics. 2010;125(4):686–95.
50. Caprio S, Daniels SR, Drewnowski A, et al. Influence of race,
ethnicity, and culture on childhood obesity: implications for pre-
vention and treatment. Diabetes Care. 2008;31(11):2211–21.
51. Cuypers K, Ridder KD, Kvaløy K, et al. Leisure time activities I
adolescence in the presence of susceptibility genes for obesity:
risk or resilience against overweight in adulthood? The HUNT
study. BMC Publ Health. 2012;12:820.
52. Cossrow N, Falkner B. Race/ethnic issues in obesity and obesity-
related comorbidities. J Clin Endocrinol Metab. 2004;89
(6):2590–4.
53. Huang RC, Burke V, Newnham J, et al. Perinatal and childhood
origins of cardiovascular disease. Int J Obes. 2006;31(2):236–44.
54. Gluckman PD, Hanson MA, Hanson CX, Thornburg KL. Effect
of in utero and early-life conditions on adult health and disease.
New England J Med. 2008;359(1):61–73.
55. Shankar K, Harrell A, Liu X, et al. Maternal obesity at conception
programs obesity in the offspring. Am J Physiol-Reg I. 2008;294
(2):R528–38.
56. • Ferraro ZM, Barrowman N, Prud'homme D, et al. Excessive
gestational weight gain predicts large for gestational age neonates
independent of maternal body mass index. J Maternal-Fetal
Neonatal Med. 2012;25(5):538–42. This paper found out that
higher pre-pregnancy BMI and gestational weight gain was
associated with increased rate of large-for-gestational-age birth
weight after controlling for maternal and gestational age, pre-
pregnancy weight, parity and smoking.
57. Yu ZB, Han SP, Zhu GZ, et al. Birth weight and subsequent risk
of obesity: a systematic review and meta-analysis. Obesity Rev.
2011;12(7):525–42.
58. Stuebe AM, Forman MR, Michels KB. Maternal-recalled gesta-
tional weight gain, pre-pregnancy body mass index, and obesity
in the daughter. International J Obes. 2009;33(7):743–52.
59. Catalano PM, Farrell K, Thomas A, et al. Perinatal risk factors for
childhood obesity and metabolic dysregulation. Am J Clin Nutr.
2009;90(5):1303–13.
60. O’Brien TE, Ray JG, Chan WS. Maternal body mass index and
the risk of preeclampsia: a systematic overview. Epidemiology.
2003;14(3):368–74.
20
61. Langer O, Yogev Y, Xenakis EMJ, Brustman L. Overweight and
obese in gestational diabetes: The impact on pregnancy outcome.
Am J Obstet Gynecol. 2005;192(6):1768–76.
62. Hull HR, Thornton JC, Ji Y, et al.: Higher infant body fat with
excessive gestational weight gain in overweight women. Am J
Obstet Gynecol. 2011;205(3):211 e1-7.
63. Schack-Nielsen L, Michaelsen KF, Gamborg M, et al. Gestational
weight gain in relation to offspring body mass index and
obesity from infancy through adulthood. Int J Obes. 2010;34
(1):67–74.
64. Ludwig DS, Currie J. The association between pregnancy weight
gain and birthweight: a within-family comparison. Lancet.
2010;376(9745):984–90.
65. Adamo KB, Ferraro ZM, Brett KE. Can we modify the intrauter-
ine environment to halt the intergenerational cycle of obesity? Int
J Environ Res Public Health. 2012;9(4):1263–307.
66. McMillen IC, Rattanatray L, Duffield JA, et al.: The early origins
of later obesity: pathways and mechanisms. Adv Exp Med Biol.
2009;71-81.
67. Levin BE. Epigenetic influences on food intake and physical
activity level: review of animal studies. Obesity. 2008;16 Suppl
3:S51–4.
68. Bayol SA, Farrington SJ, Stickland NCA. Maternal 'junk food'
diet in pregnancy and lactation promotes an exacerbated taste for
'junk food' and a greater propensity for obesity in rat offspring.
Brit J Nutr. 2007;98(4):843–51.
69. Bayol SA, Simbi BH, Bertrand JA, Stickland NC. Offspring from
mothers fed a 'junk food' diet in pregnancy and lactation exhibit
exacerbated adiposity that is more pronounced in females. J
Physiol. 2008;586(13):3219–30.
70. Schaefer-Graf UM, Graf K, Kulbacka I, et al. Maternal lipids as
strong determinants of fetal environment and growth in pregnan-
cies with gestational diabetes mellitus. Diabetes Care. 2008;31
(9):1858–63.
71. • Catalano PM, Hauguel-De Mouzon S. Is it time to revisit the
Pedersen hypothesis in the face of the obesity epidemic? Am J
Obstet Gynecol. 2011;204(6):479–87. This review article gave an
understanding of the metabolic environment of obese diabetic
women and lipid metabolism affecting fetal adiposity through
perinatal metabolic programming since these issues relates to
the increasing trends of obesity.
72. Moraeus L, Lissner L, Yngve A, et al. Multi-level influences on
childhood obesity in Sweden: societal factors, parental determi-
nants and child’s lifestyle. Int J Obes. 2012;36(7):969–76.
73. Dollman J, Norton K, Norton L. Evidence for secular trends in
children’s physical activity behaviour. Br J Sports Med.
2005;39:892–7.
74. Han JC, Lowlor DA, Kimm SYS. Childhood obesity-2010: prog-
ress and challenges. Lancet. 2010;375(9727):1737–48.
75. Chhatwal J, Verma M, Riar SK. Obesity among pre-adolescent
and adolescents of a developing country (India). Asia Pacific J
Clin Nutr. 2004;13(3):231.
76. Manios Y, Panagiotakos DB, Pitsavos CE, et al. Implication of
socio-economic status on the prevalence of overweight and obe-
sity in Greek adults: the ATTICA study. Health policy
(Amsterdam, Netherlands). 2005;74(2):224.
77. Wells JCK, Marphatia AA, Cole TJ, McCoy D. Associations
of economic and gender inequality with global obesity prev-
alence: understanding the female excess. Social Sci Med.
2012;75:482–90.
78. •• Wang Y, Lim H. The global childhood obesity epidemic and
the association between socio-economic status and childhood
obesity. Int Rev Psych. 2012;24(3):176–88. This paper not only
gave an overview of current prevalence of childhood obesity and
its association with socio-economic status, but also foreseen the
time trends of childhood obesity.
Curr Obes Rep (2013) 2:10–22
79. Chia Y. Dollars and pounds: the impact of family income on
childhood weight. Appl Econ. 2012;45(14):1931–41.
80. Arenz S, Ruckerl R, Koletzko B, von Kries R. Breast-feeding and
childhood obesity–a systematic review. Int J Obes. 2004;28
(10):1247–56.
81. Owen CG, Martin RM, Whincup PH, et al. Effect of Infant
Feeding on the Risk of Obesity Across the Life Course: A
Quantitative Review of Published Evidence. Pediatrics.
2005;115(5):1367–77.
82. Savino F, Nanni G, Maccario S, et al. Breast-fed infants have
higher leptin values than formula-fed infants in the first four
months of life. J Pedia Endocrinology and Metabol. 2004;17
(11):1527–32.
83. Disantis KI, Collins BN, Fisher JO, Davey A. Do infants fed
directly from the breast have improved appetite regulation and
slower growth during early childhood compared with infants fed
from a bottle? Int J Behav Nutr Phy. 2011;8:89.
84. Crume TL, Ogden L, Maligie M, et al. Long-term impact of
neonatal breastfeeding on childhood adiposity and fat distribution
among children exposed to diabetes in utero. Diabetes Care.
2011;34(3):641–5.
85. Pérez-Escamilla R, Obbagy JE, Altman JM, et al. Dietary energy
density and body weight in adults and children: a systematic
review. J Acad Nutr Dietetic. 2012;112(15):671–84.
86. Fulkerson JA, Neumark-Sztainer D, Hannan PJ, Story M. Family
meal frequency and weight status among adolescents: cross-
sectional and 5-year longitudinal associations. Obesity. 2008;16
(11):2529–34.
87. Rosenheck R. Fast food consumption and increased caloric in-
take: a systematic review of a trajectory towards weight gain and
obesity risk. Obesity Rev. 2008;9(6):535–47.
88. Astbury NM, Taylor MA, Macdonald IA. Breakfast consumption
affects appetite, energy intake, and the metabolic and endocrine
responses to foods consumed later in the day in male habitual
breakfast eaters. J Nutr. 2011;141(7):1381–9.
89. Eloranta A, Lindi V, Schwab U, et al. Dietary factors associated
with overweight and body adiposity in Finnish children aged 6–
8 years: the PANIC Study. Int J Obes. 2012;36(7):950–5.
90. Antonogeorgos G, Panagiotakos D, Papadimitriou A, et al.
Breakfast consumption and meal frequency interaction with
childhood obesity. Ped Obes. 2012;1:65–72.
91. • Kral TV, Whiteford LM, Heo M, Faith MS. Effects of eating
breakfast compared with skipping breakfast on ratings of appetite
and intake at subsequent meals in 8- to 10-y-old children. Am J
Clin Nutr. 2011;93(2):284–91. This study gave an insight that
over-compensation for the missing calories from skipping break-
fast by eating more among children despite differences in subjec-
tive feelings of hunger and appetite.
92. Kral TVE, Allison DB, Birch LL, et al. Caloric compensation and
eating in the absence of hunger in 5-to 12-y-old weight-
discordant siblings. Am J Clin Nutr. 2012;96(3):574–83.
93. Vasquez F, Salazar G, Andrade M, et al. Energy balance and
physical activity in obese children attending day-care centres.
Eur J Clin Nutr. 2006;60(9):1115–21.
94. van der Horst K, Oenema A, Ferreira I, et al. A systematic review
of environmental correlates of obesity-related dietary behaviors in
youth. Health Edu Res. 2007;22(2):203–26.
95. Gillis LJ, Bar-Or O. Food away from home, sugar-sweetened
drink consumption and juvenile obesity. J Am Coll Nutr.
2003;22(6):539–45.
96. Amin TT, Al-Sultan AI, Ali A. Overweight and obesity and their
relation to dietary habits and socio-demographic characteristics
among male primary school children in Al-Hassa, Kingdom of
Saudi Arabia. Eur J Nutr. 2008;47(6):310–8.
97. Neumark-Sztainer D, Story M, Hannan PJ, Croll J. Overweight
status and eating patterns among adolescents: where do youths
Curr Obes Rep (2013) 2:10–22
stand in comparison with the healthy people 2010 objectives? Am
J Public Health. 2002;92(5):844–51.
98. McGinnis JM, Gootman JA & Kraak VI: Food marketing to
children and youth: threat or opportunity? United States of
America: National Academic Press; 2006.
99. Harris JL, Pomeranz JL, Lobstein T, Brownell KD. A crisis in the
marketplace: how food marketing contributes to childhood obe-
sity and what can be done. Ann Rev Public Health. 2009;30:211–
25.
100. WHO: A framework for implementing the set of recommenda-
tions on the marketing of foods and non-alcoholic beverages to
children. Geneva, Switzerland. 2012.
101. Holick MF. Vitamin D deficiency. New England J Med. 2007;357
(3):266–81.
102. Earthman C, Beckman L, Masodkar K, Sibley S. The link be-
tween obesity and low circulating 25-hydroxyvitamin D concen-
trations: considerations and implications. Int J Obes. 2011;36
(3):387–96.
103. Bammann K, Sioen I, Huybrechts I, et al. The IDEFICS valida-
tion study on field methods for assessing physical activity and
body composition in children: design and data collection. Int J
Obes. 2011;35:S79–87.
104. Lazaar N, Aucouturier J, Ratel S, et al. Effect of physical activity
intervention on body composition in young children: influence of
body mass index status and gender. Acta Paediatrica. 2007;96
(9):1321–5.
105. Dulloo AG. Energy balance and body weight homeostasis. In:
Kopelman PG, Caterson ID, Dietz WH, editors. Clinical Obesity
in Adults and Children. Third Edition. Oxford: Blackwell; 2010.
p. 67–81.
106. Pate RR, Freedson PS, Sallis JP, et al. Compliance with physical
activity guidelines: Prevalence in a population of children and
youth. Ann Epidemiol. 2002;12(5):303–8.
107. Food and Nutrition Research Institute: Physical activity: Do
Asian children get enough? Available at http://www.fnri.dost.
gov.ph/index.php?option0content&task0view&id0704
108. Merchant AT, Dehghan M, Behnke-Cook D, Anand SS. Diet,
physical activity and adiposity in children in poor and rich neigh-
bourhoods: a cross sectional comparison. Nutr J. 2007;6(1):1.
109. Patrick K, Norman GJ, Calfas KJ, et al. Diet, physical activity
and sedentary behaviors as risk factors for overweight in adoles-
cence. Arch Ped Ado Med. 2004;158(4):385.
110. Ortega FB, Ruiz JR, Sjöström M. Physical activity, overweight
and central adiposity in Swedish children and adolescents: the
European Youth Heart Study. Int J Behav Nutr Phy Act. 2007;4
(1):61.
111. Te Velde S, Van Nassau F, Uijtdewilligen L, et al. Energy
balance-related behaviours associated with overweight and obe-
sity in preschool children: a systematic review of prospective
studies. Obes Rev. 2012;13:56–74.
112. Jimenez-Pavon D, Kelly J, Reilly JJ. Associations between ob-
jectively measured habitual physical activity and adiposity in
children and adolescents: Systematic review. Int J Ped Obes.
2010;5(1):3–18.
113. Özmert EN, Özdemir R, Pektas A, et al. Effect of activity and
television viewing on BMI z-score in early adolescents in Turkey.
World J Pediatr. 2011;7(1):37–40.
114. Temple JL, Giacomelli AM, Kent KM, Roemmich JN, Epstein
LH. Television watching increases motivated responding for
food and energy intake in children. Am J Clin Nutr. 2007;85
(2):355–61.
115. Carlson JA, Crespo NC, Sallis JF, et al. Dietary-Related and
Physical Activity-Related Predictors of Obesity in Children: A
2-Year Prospective Study. Childhood Obesity (Formerly Obesity
and Weight Management). 2012;8(2):110–5.
21
116. Metcalf BS, Hosking J, Jeffery AN, et al. Fatness leads to inac-
tivity, but inactivity does not lead to fatness: a longitudinal study
in children (EarlyBird 45). Arch Dis Child. 2011;96:942–7.
117. Reilly JJ, Kelly L, Montgomery C, et al. Physical activity to
prevent obesity in young children: cluster randomised controlled
trial. BMJ. 2006;333:1041–3.
118. • Jiang F, Zhu S, Yan C, et al. Sleep and obesity in preschool
children. J Ped. 2009;154(6):814–8. Caregivers who slept less
and mothers with higher education related to short sleep duration
of pre-school children, especially decreased bedtime sleep hours
at night. Children who slept less than <9.4 hours per night were
more likely to be obese than who slept ≥11 hours (odds ratio
[OR], 4.76; 95% CI, 1.28-17.69; P<0.05; OR, 3.42; 95% CI,
1.12-10.46; P<0.05).
119. Al Mamun A, Lawlor DA, Cramb S, et al. Do childhood sleeping
problems predict obesity in young adulthood? Evidence from a
prospective birth cohort study. Am J Epidemiol. 2007;166
(12):1368–73.
120. Cappuccio FP, Taggart FM, Kandala NB, Currie A. Meta-analysis
of short sleep duration and obesity in children and adults. Sleep.
2008;31(5):619.
121. Marshall NS, Glozier N, Grunstein RR. Is sleep duration related
to obesity? A critical review of the epidemiological evidence.
Sleep Med Rev. 2008;12(4):289–98.
122. Horne J. Short sleep is a questionable risk factor for obesity and
related disorders: statistical versus clinical significance. Biol
Psychol. 2008;77(3):266–76.
123. Taheri S. The link between short sleep duration and obesity: we
should recommend more sleep to prevent obesity. Arch Dis
Child. 2006;91(11):881–4.
124. Eisenmann JC. Insight into the causes of the recent secular trend
in pediatric obesity: Common sense does not always prevail for
complex, multi-factorial phenotypes. Prevent Med. 2006;42
(5):329–35.
125. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with
childhood obesity? A systematic review and meta-analysis.
Obesity. 2008;16(2):265–74.
126. Canapari CA, Hoppin AG, Kinane TB, et al. Relationship be-
tween sleep apnea, fat distribution, and insulin resistance in obese
children. Journal of clinical sleep medicine: JCSM. 2011;7
(3):268–73.
127. Arens R, Sin S, Nandalike K, et al. Upper airway structure and
body fat composition in obese children with obstructive sleep
apnea syndrome. Am J Resp Critical Care Med. 2011;183
(6):782–7.
128. • Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal
analysis of sleep in relation to BMI and body fat in children: the
FLAME study. BMJ. 2011;342:d2712–2. This paper showed that
the pre-school children who sleep less gain significantly more fat
mass overtime even after adjustment for multiple determinants of
body composition during growth. Each additional hour of sleep
reduced the adjusted fat mass index by 0.48 (0.10 to 0.86) for the
change from age 3 to 7.
129. Bayer O, Rosario AS, Wabitsch M, Von Kries R. Sleep duration
and obesity in children: is the association dependent on age and
choice of the outcome parameter? Sleep. 2009;32(9):1183.
130. Nielsen LS, Danielsen KV, Sørensen TIA. Short sleep duration as
a possible case of obesity: critical analysis of the epidemiological
evidence. Obes Rev. 2011;12(2):78–92.
131. Matricciani L, Olds T, Williams M. A review of evidence for the
claim that children are sleeping less than in the past. Sleep.
2011;34(5):651.
132. Morrissey TW, Dunifon RE, Kalil A. Maternal employment,
work schedules, ad children’s body mass index. Child Dev.
2011;82:66–81.
22
133. Li L, Law C, Conte RL, Power C. Intergenerational influences on
childhood body mass index: the effect of parental body mass
index trajectories. Am J Clin Nutr. 2009;89(2):551–7.
134. Oken E, Levitan E, Gillman M. Maternal smoking during preg-
nancy and child overweight: systematic review and meta-
analysis. Int J Obes. 2007;32(2):201–10.
135. Ong KKL, Preece MA, Emmett PM, Emmett ML, Dunger
DB. Size at birth and early childhood growth in relation to
maternal smoking, parity and infant breast-feeding: longitu-
dinal birth cohort study and analysis. Ped Res. 2002;52
(6):863–7.
136. Von Kries R. Maternal Smoking during Pregnancy and
Childhood Obesity. Am J Epidemiol. 2002;156(10):954–
61.
Curr Obes Rep (2013) 2:10–22
137. Jo YH, Talmage DA, Role LW. Nicotinic receptor-mediated effects
on appetite and food intake. J Neurobiol. 2002;53(4):618–32.
138. Audrain-McGovern J, Benowitz NL. Cigarette smoking, nicotine,
and body weight. Clin Pharmacol Therap. 2011;90(1):164–8.
doi:164.
139. Lerman C, Berrettini W, Pinto A, et al. Changes in food reward
following smoking cessation: a pharmacogenetic investigation.
Psychopharmacology. 2004;174(4):571–7.
140. Mindlin M, Jenkins R, Law C. Maternal employment and indi-
cators of child health: a systematic review in pre-school children
in OECD countries. J Epidemiol Comm Health. 2009;63:340–50.
141. Champion SL, Rumbold AR, Steele EJ, et al. Parental work
schedules and child overweight and obesity. Int J Obes.
2012;36:573–80.