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doi:10.1111/jpc.12819

REVIEW ARTICLE

Viewpoint article: Childhood obesity – looking back over 50 years

to begin to look forward
Matthew A Sabin,1,2 Kung-Ting Kao,1,2 Markus Juonala,3,4,5 Louise A Baur6 and Melissa Wake1,2
1
Murdoch Childrens Research Institute, The Royal Children’s Hospital, 2Department of Paediatrics, University of Melbourne, Melbourne, Victoria, 6Physical
Activity Nutrition Obesity Research Group, University of Sydney, Sydney, New South Wales, Australia, 3Research Centre of Applied and Preventive
Cardiovascular Medicine, and 4Department of Medicine, University of Turku and 5Division of Medicine, Turku University Hospital, Turku, Finland

Abstract: The last 50 years have seen the emergence of childhood obesity as a major public health concern and a condition now regularly
encountered in routine general paediatric practice. Causes are extremely complex, bringing together multifactorial environmental factors and
individual genetics, and we still do not have a clear understanding of why some children appear predisposed to exaggerated and sometimes
extreme weight gain. Overweight and obese children of today face an uncertain future. They are likely to experience higher rates of type 2
diabetes and heart disease, as well as many other health problems. However, while the prevalence of childhood obesity has progressively
increased over the last few decades, so has research into its underlying causes. This has led to large-scale trials aimed at improving prevention
or treatment. As data have emerged from such studies, we have begun to accept that the heterogeneity of obesity means that broad ‘common
sense’ strategies to address diet and activity will not lead to success on their own. Now is the time to begin to build on this information, dispelling
myths and beliefs, in order to focus research efforts and take first steps towards more sophisticated strategies that go beyond the surface
behaviours that simply potentiate obesity. Through carefully designed studies, aimed at tackling fundamental questions missed in the hasty
development of ‘common sense’ approaches, will come answers that can lead to the development of more effective community- and health-
care-orientated prevention and treatment programmes.
Key words: children; history; obesity.

For many conditions reviewed in this special edition, the last 50
years have seen unprecedented improvements in the outcome
of medical problems that have limited the health of children
over millennia. This is not the case for childhood obesity, which
can truly be called a ‘new morbidity’. In this time, its preva-
lence, but also its severity, has reached levels unimaginable at a
time when televisions, computers, fast cars and takeaway food
were an exciting vision for the future. Childhood obesity has
now become a truly global crisis, affecting children in rich and
poor countries, and is one of the world’s most pressing public
health issues.
Initial efforts by clinical and population health researchers
were in basic areas of establishing consistent definitions and
characterisation in order to develop strategies for improved
recognition. Some developed hasty ‘quick fix’ strategies using
‘common sense’ approaches but, despite promising short-term
results, all failed to curb the ensuing epidemic.1 There was also
a concomitant drive to develop a more substantial evidence
Correspondence: Dr Matthew A Sabin, Centre for Hormone Research,
Murdoch Childrens Research Institute, Flemington Road, Parkville, Vic.
3052, Australia. Fax: +61 3 9345 6240; email: matt.sabin@rch.org.au
Conflict of interest: All authors have nothing to disclose and declare no
conflict of interest, including relevant financial interests, activities, relation-
ships and/or affiliations pertaining to this work.
Accepted for publication 19 August 2014.
base regarding the complex factors leading to weight gain – a
necessary exercise, but one which probably increased confu-
sion.2 This typified an ‘early responder’, knee-jerk response to
a novel problem, lacking cohesion and structure. Thus, the
history of childhood obesity over 50 years predates the devel-
opment of effective population level prevention measures,
advanced management strategies or the development of new
drugs.
Looking back over 50 years, it is interesting to see how the
needs of children have changed. In 1965, the Nobel Peace Prize
was awarded to the United Nations International Children’s
Emergency Fund (UNICEF), now termed the United Nations
Children’s Fund. This organisation, formed in 1946 following
the Second World War, is active across 190 countries and terri-
tories. Although times have changed and the life-style and
health-care needs of many young children have altered, one of
UNICEF’s core missions still holds strong: ‘to advocate for meas-
ures to give children the best start in life, because proper care at
the youngest age forms the strongest foundation for a person’s
future’. Fifty years ago, the ‘best start to life’ meant improving
access to food, clothing and health care. Nowadays, those who
continue to face these critical needs coexist with a growing
number of children (sometimes in the same community) whose
long-term health will be affected by long-term weight problems.
In 2014, the World Health Organization (WHO) established
a high-level Commission on Ending Childhood Obesity3 to
address this latest threat to the ‘best start to life’.

82 Journal of Paediatrics and Child Health 51 (2015) 82–86

© 2015 The Authors
Journal of Paediatrics and Child Health © 2015 Paediatrics and Child Health Division (Royal Australasian College of Physicians).
MA Sabin et al.
Fig. 1 Prevalence of overweight and obesity for 5–15-year-old Australian
children. Lines of best fit (third order polynomial) are shown for all data
combined (r2 = 0.83; root mean square residual (RMSR) 2.2%) and for raw
data only (r2 = 0.75, RMSR = 3.3%). Open circles are age- and gender-specific
prevalence rates based on descriptive data. Filled circles are derived from
raw data. Each circle represents an age and gender slice for a single study.
Reproduced with permission from Norton et al.7
There is little to suggest obesity was common in society until
the last 50 years, despite evidence for obesity in our prehistoric
ancestors.4 Data from the National Health Examination Survey
undertaken in the United States in the 1960s indicate that only
around 4–5% of children were overweight at that time.5,6 In
Australia, the prevalence of overweight and obesity in school-
aged children was relatively constant throughout most of the
20th century, but rose from the 1970s (Fig. 1).7 Since then,
there has been a steady increase in the prevalence of overweight
and obesity, which has risen by approximately 5% per decade in
most developed countries.8 Recently, however, increases have
been less dramatic9 and some reports suggest a plateauing across
several countries.10
Despite this, current figures indicate that across the developed
world, >20% of children are now overweight or obese, with
America recording rates of approximately 32%.11 However,
there are sometimes significant inter-country differences in
reported rates, as a result of the use of different recognised
cut-points (mainly WHO, International Obesity Task Force and
US Centers for Disease Control and Prevention).
What Have We Learned over the Last
50 Years about the Causes of
Childhood Obesity?
Environmental causes for obesity are complex but at a macro-
scopic level are based around a chronic imbalance between
energy intake and energy expenditure. This imbalance involves
many factors, including easy access to energy-dense foods,
increased portion sizes, reduced physical activity and increased
time in sedentary activities. At a daily level, these imbalances
may be very small, and their environmental cues slightly off
balance, yet together they may potentiate weight gain over many
Journal of Paediatrics and Child Health 51 (2015) 82–86
© 2015 The Authors
Journal of Paediatrics and Child Health © 2015 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Fifty years of childhood obesity
years. Measurement of most of the postulated culprits however –
such as fast food, TV/computers and sugar-sweetened beverages
– remains very inexact and it has been difficult to tease out the
role of putative specific life-style factors across groups of very
different people. This problem has also been compounded on
occasion by marked conflicts of interest in reporting.12
There is also substantial evidence for a strong genetic compo-
nent to the determination of body composition in young chil-
dren.13 Some ‘obesity genes’ have been identified but each is
likely to play only a small role and there is still a large gap
between the evidence for genetic regulation of weight and
actual identified genes.14 Furthermore, evolving research in
epigenetics suggests that environmental triggers may affect the
expression of some key weight-regulating genes.15
With these studies, we have increased our understanding of
how the body regulates energy and promotes weight gain.
However, much of this work has been in mature animal models
or obese adults, and physiology of weight regulation in children
is relatively under-explored. Childhood is the only period in life
when body mass index (BMI; kg/m2) inflection points are the
norm, with a peak at around 12 months, a nadir around 5–6
years (the period of adiposity rebound) and a further upward
inflection around puberty. Thus, the body reduces adiposity
during the pre-school years, while maintaining a steady rate of
skeletal and muscular growth. Learning more about what con-
trols this process may increase our understanding of factors that
protect against obesity.16
Furthermore, the role of recently discovered hormones in the
development of obesity in childhood is still to be elucidated.
Leptin (first described in 1994, although studies had suggested
its existence for decades before) is the major hormone produced
from white adipose tissue and acts principally in the hypothala-
mus to influence satiety (although it also has other important
roles in reproduction and bone health).17 Leptin, and other
associated ‘satiety’ hormones (such as ghrelin and other hor-
mones produced from the gastrointestinal tract that act on the
central nervous system to control hunger), is now thought to
regulate weight tightly by determining a set-point, which is
vehemently defended in adult life.18 How these set-points are
determined, the role of satiety hormones in their defence and
their impact on variations in childhood growth and weight gain
are currently unknown.
Childhood obesity is also a topic that sparks strong and
sometimes seemingly visceral reactions – everyone has an
opinion. Unsurprisingly, therefore, the science of treatment
and prevention is beset by both presumptions (persistent
beliefs in the absence of supporting scientific evidence) and
myths (persistent beliefs despite contradictory evidence). The
former includes examples such as ‘regularly eating breakfast
protects against obesity’ and ‘snacking contributes to weight
gain and obesity’, while the latter includes advice such as slow
weight loss has greater long-term benefit than rapid weight
loss, breastfeeding protects against obesity and even that
sexual activity burns enough calories to aid weight loss.19,20
Researchers, who belong to society as well as science, are far
from immune to these beliefs. In fact, ‘white hat bias’ in the
findings that researchers and/or journal editors/reviewers may
subconsciously and selectively promulgate is a further hin-
drance to progress.21
83
Fifty years of childhood obesity
What Have We Learned over the Last
50 Years about How to Prevent
Childhood Obesity?
Given the complexity, it is perhaps not surprising that there
have been major challenges in implementing effective preven-
tion strategies.22 There is growing evidence of the effectiveness
of whole-of-school and community-based interventions to
promote improvements in children’s eating and activity pat-
terns, although few such interventions lead to changes in body
fatness.23 In many developed countries, a range of broader,
upstream strategies have been recommended as part of a
co-ordinated multi-level approach to obesity prevention.24 The
suite of suggested strategies includes the regulation of marketing
of unhealthy foods, improved food labelling, better access to
affordable fruits and vegetables in rural and remote regions,
taxes on unhealthy foods and changes in urban infrastructure to
promote active transport and provide recreation space. Such
approaches require strong political will and broad community
support. In Australia and New Zealand, there has been some
progress in implementing smaller scale programmes and social
marketing, but little action on these broader public policy
approaches that promote healthy eating and physical activity.22
What Have We Learned over the Last
50 Years about the Health-Related
Consequences of Childhood Obesity and
How Should They Best Be Managed?
Although manuscripts from the 1950s reported how childhood
obesity should be managed in paediatric practice25 and more
comprehensive reviews emerged in the 1960s and 1970s, evi-
dence for the clear relationship between childhood obesity and
later disease really first emerged from studies in Pima Indians,26
and then the Bogalusa Heart Study in the United States.27 Since
that time, research into the links between childhood obesity and
later disease has grown at a rate similar to the prevalence of
childhood obesity itself. The US National Library of Medicine
(PubMed) lists 10 papers on ‘childhood obesity’ in 1965, 84
papers in 1995 and 1066 papers in 2013, and there is now
substantial evidence demonstrating the detrimental effects of
childhood obesity on health.28 The major problem with child-
hood obesity is that obesity tracks strongly over time, so many
of today’s overweight and obese children will grow up to be
tomorrow’s overweight and obese adults, increasing the public
health burden of adult obesity. In 2010, adult obesity was esti-
mated to cost the Australian economy $56.6 billion.29 However,
childhood obesity has definite detrimental effects on health,
both short and long term, including an increased risk of type 2
diabetes, heart and liver disease, obstructive sleep apnoea, joint
and mobility issues and a diverse array of short- and long-term
psychosocial issues.30
Some of the evidence for the longer term health problems of
childhood obesity emerged from large-scale longitudinal epide-
miology studies set up in the late 1970s, such as the Cardiovas-
cular Risk in Young Finns Study,31 which collected data on hard
outcomes in adulthood. The problem, of course, is that to
answer today’s questions, we may need to develop studies and
then possibly wait another 50 years before we have ‘hard’
84
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MA Sabin et al.
outcomes. It is imperative therefore that we design and perform
studies comprehensive enough to allow us to look at ‘hard’
intermediate quantitative outcomes in later childhood, adoles-
cence and early adult life. These are now being developed at a
community-based level (such as the Child Health CheckPoint,
being run through the Longitudinal Study of Australian Chil-
dren32) and in those with established obesity (such as the Child-
hood Overweight BioRepository of Australia33).
The explosion in childhood obesity research has been fol-
lowed by the development of comprehensive evidence-based
guidelines for the clinical management of childhood obesity.34
The Australian National Health and Medical Research Council
has published ‘Clinical Practice Guidelines for the Management
of Overweight and Obesity in Adults, Adolescents and Children
in Australia’,35 which supports a comprehensive initial assess-
ment followed by education and support aimed at family-
focused life-style change, with only those adolescents with
severe obesity and health-related complications being consid-
ered for pharmacotherapy or surgery. Importantly, however,
they also begin to address the diversity in the causes of
obesity and the need for different management needs between
individuals.
In terms of pharmacotherapy, the sad story of the paucity of
drug development for adult obesity means we have only one
rather unpalatable pharmacotherapeutic option (orlistat) avail-
able for obese adolescents who fail life-style change.36 Bariatric
surgery in adolescents is a contentious area with debate about
the most appropriate technique and the most appropriate
patients.37,38 Is bariatric surgery better in a severely obese ado-
lescent with little/no health-related complications or in an ado-
lescent with mild obesity who also has type 2 diabetes,
hypertension and fatty liver disease? These are difficult clinical
conundrums at a time when bariatric surgery cannot, and
should probably not, be offered to all those who seek it. It is
concerning that in most countries (including Australia and New
Zealand), so few services are available at a primary, secondary or
tertiary care level that can offer obesity management in a logical
sequence (life-style measures before pharmacotherapy/surgery)
and through the recommended multidisciplinary format. A cor-
ollary is the need for a health workforce trained better in the
assessment and management of paediatric obesity.
There remains a paucity of good-quality evidence relating
to key aspects of paediatric obesity management. Examples
include:
1 Paediatricians being at the forefront in the clinical manage-
ment of obese children and adolescents, yet a recent survey
found that while most felt very/quite competent in assessing
(89%) and managing (68%) obesity, few (20%) felt they
would be able to make a difference (20%) or appropriately
manage comorbidities (21–45%).39
2 Recommendations on the clinical management of overweight
and obese youth being based on common sense and a com-
prehensive (but limited) evidence base,40 but many questions
remaining as to appropriate investigations and recommenda-
tions. For example, many practitioners routinely measure
fasting insulin levels in overweight and obese children. Yet
they are a poor surrogate measure for insulin sensitivity and
high levels are not associated with the development of type 2
diabetes.41 Furthermore, we do not know how much change
Journal of Paediatrics and Child Health 51 (2015) 82–86
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MA Sabin et al.
in physical activity and diet in young obese children is needed
to induce weight change.
3 While overweight and obese youth who grow up to be non-
obese adults have the same risks of type 2 diabetes and risk
factors for heart disease in adult life as those who have never
been obese,42 it is unclear how this finding translates to clini-
cal practice. We do not know how much weight change in
obese youth will be associated with improvements in long-
term health.
4 How can we best train and upskill those who see overweight
and obese children/adolescents in clinical practice? How
much can reasonably be addressed at a primary level, which
children or adolescents should be referred to specialist
services and how should specialist services be funded and
structured?
5 How should obesity be best prevented and treated in cultur-
ally and linguistically diverse communities, the socially
disadvantaged and youth in remote and/or resource-poor
communities? As obesity so often affects these individuals and
their families, it is important to design research studies appro-
priate to these settings that can provide realistic solutions.
What Will the Next 50 Years Bring for the
Overweight and Obese Children of Today?
Unless there is a sudden and unexpected decline in the preva-
lence of childhood obesity, large numbers of currently obese
youth will grow up to be obese adults with the major attendant
health risks. Approximately one in four obese children and
adolescents display a clustering of cardiovascular risk factors
termed the ‘metabolic syndrome’,43 which increases their
medium term chance of heart disease by a factor of 10.44
Furthermore, approximately 1 in 10 obese children have pre-
diabetes,43 which progresses to type 2 diabetes as weight con-
tinues to increase.45 The only long-term follow-up study of
individuals who developed obesity-related type 2 diabetes in
adolescence found that within 15 years of diagnosis, 1 in 20
needed permanent kidney dialysis and 1 in 10 was dead.46
Fortunately, it appears likely that the prevalence of childhood
obesity will not continue to rise much higher. Recent data
suggest a stabilisation in prevalence across many developed
countries,47 although the severity of obesity may continue to
worsen.48 This will likely lead to an up-swing in the rates of
severely obese adolescents referred for bariatric surgery; it is
imperative that national registers are established quickly to
record outcome following different forms of surgical treatment.
Furthermore, it will be necessary to undertake careful evalu-
ation of any new anti-obesity drugs in adolescents, especially if
indicated only for the treatment of adults. When considering
pharmacotherapy, is there a major difference between a
15-year-old post-pubertal adolescent and a 19-year-old, if
both have a BMI of 50 kg/m2 and major obesity-related health
problems?
Fundamental questions about childhood obesity remain. Does
enhanced physical activity in childhood lead to overall benefits
to BMI, as well as to cardiovascular health?49 Can we regulate
how children and adolescents eat?50 Should we be looking for
other factors in childhood, such as poor sleep quality, which
may be responsible for increased food intake51 and even reduce
Journal of Paediatrics and Child Health 51 (2015) 82–86
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Journal of Paediatrics and Child Health © 2015 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Fifty years of childhood obesity
a child’s ability to exercise?52 Is it time to accept that targeting
surface behaviours is unlikely to reduce childhood obesity either
for individuals or society?53 This would free us to move in new
and possibly crucial directions. For example, we could investi-
gate circumventing our innate drive to eat more and do less by
combinations of ‘nudge’ interventions and judicious legislation
and social engineering.
Fast-forward to 2065. Will there still be major global concern
around childhood obesity? Probably yes, as there appears to be
no easy solution for this extremely complex and heterogeneous
chronic disease. Will we be any further forward in being able to
understand the causes and consequences of childhood obesity,
and thus develop effective community approaches at prevention
and ‘personalised’ approaches to treatment? Hopefully.
Acknowledgements
Research at the Murdoch Children’s Research Institute is sup-
ported by the Victorian Government’s Operational Infrastruc-
ture Support Program. The National Health and Medical
Research Council supported MAS (Health Professional Training
Fellowship 1012201) and MW (Senior Research Fellowship
1046518).
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