Clinical Section / Viewpoint
Gerontology 2014;60:222–228
DOI: 10.1159/000356023
Age-Related Consequences of Childhood
Obesity
Megan M. Kelsey a Alysia Zaepfel a Petter Bjornstad b Kristen J. Nadeau a
a
Division of Pediatric Endocrinology, and b Department of Pediatrics, University of Colorado Denver, Aurora, Colo., USA
Key Words
Childhood obesity · Metabolic syndrome · Type 2 diabetes
Abstract
The severity and frequency of childhood obesity has in-
creased significantly over the past three to four decades. The
health effects of increased body mass index as a child may
significantly impact obese youth as they age. However,
many of the long-term outcomes of childhood obesity have
yet to be studied. This article examines the currently avail-
able longitudinal data evaluating the effects of childhood
obesity on adult outcomes. Consequences of obesity in-
clude an increased risk of developing the metabolic syn-
drome, cardiovascular disease, type 2 diabetes and its asso-
ciated retinal and renal complications, nonalcoholic fatty
liver disease, obstructive sleep apnea, polycystic ovarian
syndrome, infertility, asthma, orthopedic complications,
psychiatric disease, and increased rates of cancer, among
others. These disorders can start as early as childhood, and
such early onset increases the likelihood of early morbidity
and mortality. Being obese as a child also increases the likeli-
hood of being obese as an adult, and obesity in adulthood
also leads to obesity-related complications. This review out-
lines the evidence for childhood obesity as a predictor of
adult obesity and obesity-related disorders, thereby empha-
sizing the importance of early intervention to prevent the
onset of obesity in childhood. © 2014 S. Karger AG, Basel
© 2014 S. Karger AG, Basel
0304–324X/14/0603–0222$39.50/0
E-Mail karger@karger.com
www.karger.com/ger
Received: January 14, 2013
Accepted: September 17, 2013
Published online: January 9, 2014
Introduction
Childhood obesity, defined as a body mass index
(BMI) above the 95th percentile for age and sex, has
increased in severity and frequency in the United States,
Europe and Australia over the last four decades [1–4]. In
2010, more than one third of children and adolescents
in the United States were overweight or obese [4]. Fur-
thermore, over 40 million preschool children worldwide
were estimated to be overweight or obese in 2010, which
represents a 60% increase since 1990 [5]. Therefore, child-
hood obesity and its consequences are now global health
concerns. As childhood obesity appears to track over time
[6], the impact of rising pediatric obesity rates, if left un-
checked, will presumably translate to worsening rates of
obesity in adulthood in the future. The rising incidence of
adult obesity is clearly of concern, as obesity in adulthood
is known to increase the likelihood of developing cardio-
vascular disease (CVD), type 2 diabetes (T2D) and its as-
sociated retinal and renal complications, nonalcoholic
fatty liver disease (NAFLD), asthma, obstructive sleep ap-
nea (OSA), polycystic ovarian syndrome (PCOS), infer-
tility, orthopedic complications, psychiatric disease, can-
cer and other obesity-related disorders (fig. 1) [7]. While
additional, large, long-term longitudinal studies are nec-
essary to more completely understand the impact of
childhood obesity on future health outcomes, several lon-
gitudinal cohort studies discussed in this paper do suggest
that childhood obesity carries an additional increased risk
128.111.121.42 - 2/26/2018 3:20:51 AM
Univ. of California Santa Barbara
Kristen Nadeau, MD, MS
Division of Pediatric Endocrinology
University of Colorado Denver/Children’s Hospital Colorado
13123 East 16th Avenue, B265, Aurora, CO 80045 (USA)
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E-Mail kristen.nadeau @ childrenscolorado.org
 Color version available online
Genetics ‡ T2D
‡ Metabolic syndrome
Endocrino
‡ PCOS
pathies ‡ Infertility

‡ Hypertension
Cardiovas- ‡ Coronary artery
cular disease
Childhood disease ‡ Vascular complica-
Epigenetics tions of diabetes
obesity

‡ NAFLD
Misc. ‡ Hormone-influenced
obesity- cancers
related ‡ OSA
disorders ‡ Depression, anxiety

Environmental Adult
factors obesity

Fig. 1. Childhood obesity and adult com-

plications.

for adult morbidity and mortality, independent of cur-
rent adult BMI.
In addition to sequelae later in life, childhood obesity
also has known acute consequences during childhood.
Most notably, obesity-associated disorders, such as dys-
lipidemia, hypertension, NAFLD, PCOS, OSA and T2D,
that previously were only found in older adults, are now
seen commonly in children, especially during adoles-
cence (fig. 1) [7, 8]. For example, in the Treatment Op-
tions for Type 2 Diabetes in Adolescents and Youth
(TODAY) study, which included 699 obese youth (mean
age 14 years) with T2D, the prevalence of other compli-
cations of obesity was also high, including: blood pres-
sure above the 90th percentile (26.3%), blood pressure at
or above the 95th percentile (13.6%), microalbuminuria
(13%), low high-density lipoprotein cholesterol (HDL-C;
79.8%), and high triglycerides (10.2%) [9]. The onset of
these complications in childhood raises significant con-
cerns about short-term health outcomes in these youth
and their chronic health implications over time. Particu-
larly troublesome is the potential emergence at younger
ages of health issues typically seen in the geriatric popu-
lation, and as a result, earlier morbidity, mortality and a
reduction in quality of life and in overall lifespan. For
example, many complications of T2D are related to dia-
betes duration. Therefore, when T2D develops in child-
hood, the early onset predicts early complications such as
renal failure and cardiovascular events. Due to the wide-
spread nature of the obesity epidemic and the numerous
obesity-related health problems, it has been projected
that the life expectancy in the United States may decline
by up to ¾ year, an effect greater than caused by acciden-
tal deaths [10]. However, because the childhood obesity
epidemic is relatively recent, few longitudinal studies
with long-term follow-up yet exist to determine the true
impact of the rise in obesity, particularly childhood obe-
sity, on long-term mortality. This review will focus, where
at all possible, on the existing longitudinal evidence re-
garding childhood obesity, related comorbidities and
their consequences for adult disease.
Contributors to Childhood Obesity
Family history is recognized as an important risk fac-
tor for obesity [11], with evidence of approximately 50%
heritability, based on data from twin and family studies
[12]. Until recently, very little of the genetic influence
on  childhood adiposity could be explained. However,
last year, Llewellyn et al. [13] demonstrated via genome-
wide complex trait analysis a method which estimates the
total additive genetic influence due to common single-
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Obesity DOI: 10.1159/000356023
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nucleotide polymorphisms (SNPs), that 30% of the vari-
ance of BMI in twin-analysis can be explained by SNPs.
These findings underline the importance of genetics in
the development of obesity (fig. 1) and support the con-
vention of targeting children of obese parents for early
preventive interventions, as these children are at in-
creased risk of obesity [14].
In addition to genetics, the environment a child is ex-
posed to (fig. 1) is also critical, as clearly the recent global
increases in BMI cannot be entirely explained by genetics
due to the rapid pace of change. From animal models, in
which genetics versus environment is more easily manip-
ulated, we have learned much about the important role
environmental factors play in the development of child-
hood obesity. For example, Roberts et al. [15] recently
reported that inactive juvenile rodents demonstrate insu-
lin resistance, leptin resistance, NAFLD and endothelial
dysfunction when compared to their genetically similar
littermates allowed to be physically active. Furthermore,
when genetically similar littermates are offered a ‘western
diet’ versus standard chow, but allowed the same access
to physical activity, those fed the ‘western diet’ develop
early obesity [16]. Thus, obesity clearly also results from
an environmental imbalance between energy intake and
energy expenditure, with a consequent excess in adipose
tissue. Moreover, the obesity-related environmental and
genetic factors also interact in terms of epigenetic chang-
es (fig.  1). For example, the in utero environment of a
woman with obesity or gestational diabetes differs in
terms of levels of glucose, free fatty acids, insulin, inflam-
matory markers, and other factors which impact the de-
veloping fetus. Such environmentally induced epigenetic
alterations have been shown to impact both current and
future generations [17].
Gender also plays an important role in childhood obe-
sity. Boys and girls, especially once puberty begins, differ
in body composition, patterns of weight gain and in risks
for obesity-related endocrinopathies [18]. Girls are re-
ported to have greater adiposity, more insulin resistance,
lower leptin levels, lower levels of physical activity, and to
receive more benefit from physical activity than age-
matched boys [18]. In addition, in the large TODAY
study of T2D mentioned above, 65% of T2D youth iden-
tified were female, showing that early-onset obesity-relat-
ed T2D has a female predominance [9]. These data raise
particular concerns about adult outcomes in obese fe-
males. In addition, when obesity-related complications
such as T2D occur prior to pregnancy, the offspring is
then exposed to an abnormal intrauterine environment,
increasing the risk of obesity and metabolic complica-
224 Gerontology 2014;60:222–228
DOI: 10.1159/000356023
tions in future generations. Therefore, the presence of
obesity and its complications in girls prior to the age of
childbearing puts the next generation at risk. In contrast,
obese boys in the TODAY study had more hypertension
than girls [9], and adult males are known to develop more
obesity-related hypertension and coronary heart disease
than females. NAFLD and OSA are also more common
in obese boys than girls [19]. Therefore, there is also a ris-
ing concern for early heart and liver disease in men who
were obese as boys.
Tracking of Childhood to Adult Obesity
Increasing evidence suggests that obese children do
not ‘grow into’ their weight and, in fact, BMI tends to
track over time. Singh et al. [6] recently reviewed 25 pub-
lications and found consistent evidence of childhood obe-
sity tracking into adulthood. For example, in the Prince-
ton Follow-Up Study, 63% of participants who were la-
beled as ‘at risk of overweight’ (now categorized as
overweight with current terminology) as children were
obese 25 years later [20]. It is possible, however, as sug-
gested by a recent study by Juonala et al., that increased
adult disease risk associated with childhood obesity oc-
curs solely because most obese children remain obese as
adults [21]. This study combined data from four prospec-
tive cohort studies, and only those children who remained
obese as adults had increased risk for hypertension, dys-
lipidemia, CVD and T2D [21]. Nonetheless, another re-
cent longitudinal study of Israeli military draftees dem-
onstrated that higher BMI in adolescence was associated
with coronary heart disease, independent of adult BMI
[22]. Conversely, the association between childhood BMI
and diabetes in the Israeli study was lost after adjusting
for adult BMI [22]. Of note, however, the highest adoles-
cent decile of BMI in the Israeli study was only a mean of
27.6. Therefore, this cohort may not be heavy enough in
terms of weight to see the full independent impact of
childhood obesity on adult diabetes outcomes. The Israeli
study also implied that milder BMI abnormalities in
childhood may be sufficient to independently impact
CVD. In contrast, a systematic review by Lloyd et al. [23]
found little evidence to support childhood BMI as an in-
dependent risk factor for adult blood pressure or carotid
intima-media thickness, but did find an association with
these risk factors if BMI tracked from childhood to adult-
hood. Many of the existing studies rely on surrogate
markers such as blood pressure or carotid intimal medial
thickness, as opposed to the ‘hard outcomes’ of actual car-
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diovascular events or death, or lack subjects with severe,
complicated childhood obesity. Thus, there is insufficient
evidence to conclude whether childhood BMI alone influ-
ences critical adult outcomes independent of adult BMI,
especially when childhood BMI elevations are milder or
exist in the absence of other childhood obesity-related co-
morbidities. As the incidence and severity of pediatric
obesity has only increased over the past few decades, the
full impact of childhood obesity on adult outcomes is yet
to be determined. Regardless of whether pediatric obesity
has independent effects on adult disease, obesity once es-
tablished is difficult to reverse, and this persistence argues
for aggressive prevention.
Risk Factors for Future CVD
Metabolic Syndrome
The metabolic syndrome is an insulin resistance-relat-
ed set of clinical characteristics known to increase the risk
of CVD, T2D, and mortality in adults. Accepted defini-
tions of metabolic syndrome in adults encompass a com-
bination of risk factors, including increased waist circum-
ference, hypertension, hypertriglyceridemia, hyperglyce-
mia and low HDL-C. Pediatric metabolic syndrome
definitions are based on derivations of adult definitions
using age- and sex-based percentiles, rather than disease
outcomes. In the Young Finns study, a large population-
based longitudinal project, 2,195 subjects, (aged 3–18
years at baseline in 1980), were reexamined in 2001 as
adults (aged 24–39 years) [24]. Youth obesity was the
strongest risk factor for metabolic syndrome and was as-
sociated with the development of adult metabolic syn-
drome, independent of other risk factors (e.g. presence of
metabolic syndrome components in childhood) [24].
Furthermore, the Princeton Lipid Research Clinic Fol-
low-Up Study, which included 771 5- to 19-year-olds fol-
lowed up an average of 25 years later (mean age of 38.4
years), determined that pediatric metabolic syndrome
and pediatric BMI are significant predictors of adult met-
abolic syndrome [20].
Based on these studies, it may be inferred that child-
hood obesity and metabolic syndrome are direct predic-
tors of adult CVD risk, although follow-up at older ages
is necessary to definitively draw this conclusion. More-
over, beyond CVD markers, longer-term follow-up to de-
termine the age bracket at which cardiovascular events
actually occur following childhood obesity is also needed
to further define the impact of pediatric obesity and
metabolic syndrome on adult morbidity and mortality.
Age-Related Consequences of Childhood
Obesity
Hypertension and Other CVD Markers
High blood pressure, a common obesity-related health
problem, is an independent risk marker for CVD, and its
prevalence in youth appears to be increasing along with
the rising obesity rates [25]. Additionally, a meta-analysis
of 50 studies following blood pressure over time suggest-
ed that blood pressure has a tendency to track from child-
hood to adulthood [25]. This further demonstrates the
early onset of adult disease risk in obese youth, which ap-
pears to persist into adulthood.
Multiple large population-based longitudinal studies,
such as the Muscatine Study tracking from childhood to
middle-age [26, 27], demonstrate that childhood obesity
predicts the presence of noninvasive markers of adult
CVD risk. For example, high adolescent BMI was
associated with higher rates of both coronary artery
calcification [27] and carotid intimal medial thickness, a
noninvasive marker of atherosclerosis [26], in young
adult participants of the Muscatine study. Similarly,
childhood BMI was found to be predictive of young adult
carotid intimal medial thickness in 2,283 participants of
the Cardiovascular Risk in Young Finns Study [28].
Obesity in early childhood is also associated with
increasing rates of PCOS, and the presence of PCOS in
youth is linked to the presence of hypertension and carotid
intima media thickness [29]. Furthermore, retrospective
cohort studies suggest that elevated childhood BMI is
associated with higher risk for coronary heart disease [30]
and premature death [31]. Perhaps the most convincing
evidence for the association between childhood obesity
and early risk for CVD is the presence of atherosclerosis
itself found on autopsy studies of adolescents, and the fact
that the extent of atherosclerosis was strongly associated
with the presence of obesity [32]. Again, longer-term
follow-up is needed to best assess ultimate CVD outcomes.
Type 2 Diabetes
With the increasing prevalence of childhood obesity, a
larger proportion of youth diagnosed with diabetes now
have T2D, especially among youth who are considered
low-income or of minority race or ethnicity [9]. There-
fore, due to the known complications in people with T2D,
a greater focus has been placed on understanding factors
influencing the development of T2D at younger ages. The
National Longitudinal Survey of Youth study compared
the degree and duration of self-reported overweight sta-
tus with the risk for self-reported diabetes in 8,157 ado-
lescents and young adults (ages 14–21 years), from 1981
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through 2006 [33]. A higher level of excess BMI-years was
significantly associated with an increased risk of diabetes
[33]. While limited by use of self-reported data without
specification of diabetes type, this finding not surprising-
ly argues to target preventive efforts toward those with the
longest duration of overweight/obesity. Interestingly, for
a given level of excess BMI-years, younger, and Hispanic
and black individuals had even higher risks of developing
diabetes [33]. This latter finding suggests that diabetes-
related public health interventions should target younger
adults, and stands in contrast to previous dogma that
increasing age is a critical risk factor for development of
diabetes. Thus, it is possible that exposure to obesity and/
or its comorbidities at a young age has a different impact
than exposure at an older age, an area in need of further
research.
In the Princeton Follow-Up Study (822 schoolchildren
aged 6–18 years at entry), predictors of T2D in adulthood
were assessed. Childhood systolic blood pressure, BMI in
the top fifth percentile and black race predicted T2D at
age 39 years [34]. In addition, if childhood BMI, systolic
blood pressure, and diastolic blood pressure were all be-
low the 75th percentile, the risk of a young adult develop-
ing T2D 22–30 years later was only 2%, which was 5 times
lower than those with increased BMI [34]. This study pro-
vides further evidence that elevated BMI in childhood
negatively impacts adult disease development.
In addition to the possibly higher likelihood of devel-
oping T2D in younger obese subjects, the course of T2D
in some youth may be more aggressive than in older
adults. This rapid decline in β-cell function makes the
treatment of the increasing number of children diag-
nosed with T2D more difficult than in adults. For exam-
ple, children have greater failure rates than adults when
using oral therapy with metformin alone, making them
more likely than adults to require insulin-based treat-
ment [35]. Being diagnosed with T2D as a child also in-
creases the chance of developing other complications
early in life. Compared to an average 20-year-old without
T2D, a 20-year-old with T2D has on average 15.5 fewer
years of life expectancy [36]. This drastically reduced life
expectancy can be explained by microvascular and mac-
rovascular complications in those with T2D [36]. For ex-
ample, renal failure associated with diabetic nephropa-
thy is a potentially lethal complication that is reported to
develop in at least 10% of young adults who were diag-
nosed with T2D as a child [10]. Moreover, the risks of
these complications, as well as the risk of mortality from
a T2D-related comorbidity increase with age. More
studies are required to fully evaluate the differences
226 Gerontology 2014;60:222–228
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between the complications of late- versus early-onset
T2D, and the ultimate outcomes of those who develop
T2D as youth.
Obesity and Cancer
While higher BMI during adulthood is clearly linked
with certain types of cancer, including breast, ovarian and
colon cancers, much less is known about the impact of
childhood obesity on future development of cancer.
Obese girls are thought to have earlier onset of puberty,
and early pubertal development has been shown to be as-
sociated with an increase in hormonally influenced can-
cers in adulthood, including breast cancer [37]. More-
over, obesity in a prepubescent girl is associated with an
increased risk for breast cancer after menopause, even af-
ter controlling for the adult woman’s current BMI [37].
Obesity-related PCOS leads to anovulation, which may
also increase risk for endometrial hyperplasia and endo-
metrial cancer in adulthood [38]. In addition to increas-
ing the risk for developing certain cancers, high BMI has
also been associated with poor oncological outcomes
[39]. In adults, some studies also suggest that lowering
BMI can significantly improve the survival rate in some
types of cancer [39]. Thus, entering adulthood at an
already obese BMI may increase the rates of some types
of cancer and worsen survival rates once a cancer is
contracted, all areas in need of further research.
Nonalcoholic Fatty Liver Disease
Nonalcoholic fatty liver disease is defined as the pres-
ence of hepatic steatosis in the absence of alcohol use, and
can progress to hepatic inflammation, fibrosis, cirrhosis
and hepatocellular carcinoma [19]. Obesity significantly
increases the risk for NAFLD [19]. NAFLD also affects
the pediatric obese population in large numbers; the esti-
mated prevalence of NAFLD is 2.6% in normal-weight
pediatric patients compared to 53% in obese youth [19].
Pediatric NAFLD presents differently than adult NAFLD,
with unique biopsy findings, higher reported rates of fi-
brosis and cirrhosis than in adults, and highest incidence
currently reported in Hispanic boys [19]. In comparison
with children without NAFLD, children with NAFLD
have a 13.6-fold higher chance of mortality or need for
liver transplant [19]. Thus, NAFLD provides another ex-
ample in which childhood obesity is associated with poor
adult outcomes, where significant, persistent disease is al-
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ready present in adolescence and strongly associated with
increased morbidity and mortality in adulthood. Little is
known about the impact of the unique pediatric NAFLD
phenotype as obese children become adults and fail to
improve their BMI. Currently, no therapies other than
weight loss show clear benefit in youth, and longitudinal
research in larger sample sizes is needed to understand
the differences between pediatric and adult NAFLD and
to better prevent early-onset liver disease and its sequelae
in adulthood.
Comment
Adults who were obese as youth, even when control-
ling for adult BMI, have been shown to have a higher risk
of cardiac events as well as early mortality [22]. However,
the exact independent effects of childhood obesity are
difficult to tease out due to the strong correlation be-
tween BMI in childhood and BMI in adulthood. Regard-
less, childhood obesity is difficult to treat. Therefore,
obese children have a high likelihood of adult obesity and
its associated multitude of complications. Many studies
show a strong independent association between adult
BMI and mortality [40]. In particular, in a study of over
1 million adults in the United States, the lowest death
rates were reported among men with a BMI between 23.5
and 24.9 and women with a BMI of between 22.0 and
23.4, and the risk of death from all causes, CVD, cancer,
or other diseases increased throughout the range from
moderate to severe overweight for both men and women
and in all age groups [40].
As a generation of children grows up with the obesity
epidemic, they will have health risks never before consid-
ered, including early-onset T2D and its associated retinal
and renal comorbidities, CVD, PCOS, NAFLD, OSA, or-
thopedic problems, psychiatric illness and increased rates
of certain cancers, unless preventative action is taken. In
particular, the T2D-related need for dialysis and renal
transplants, and the NAFLD-associated need for liver
transplants will increase and occur at younger ages and
decrease the supply of healthy organs available for organ
donation. If projections based on current tracking of obe-
sity over time and the current prevalence of coronary
heart disease attributable to obesity are correct, the prev-
alence of coronary heart disease could reach 16% by 2035
[41]. In addition, as the current population of obese chil-
dren continues to age, the increases in obesity-related
deaths not associated with CVD have also been predicted
to increase by 4% each year [41]. All of these factors will
increase medical costs and burdens to the health care
system.
Early intervention has the most potential for prevent-
ing obesity and other long-term health consequences in
high-risk children. For example, 4-year-olds at risk for
obesity based on income, minority status, and child be-
havior problems, received family intervention aimed to
promote effective parenting and prevent behavior prob-
lems. The intervention group had lower BMI and blood
pressure, and more time spent doing physical activity dur-
ing adolescence [42] than the control group. This study
suggests that early prevention of obesity in high-risk chil-
dren holds promise, and that these efforts may contribute
to the reduction of obesity and health disparities [42].
Thus, with our current extremely high rates of obesity and
its related complications, widespread change is required.
Nearly all children need to be considered at risk for later
adult obesity, and targeted early with preventive efforts.

References
1 Ogden CL, Kuczmarski RJ, Flegal KM, Mei Z,
Guo S, Wei R, Grummer-Strawn LM, Curtin
LR, Roche AF, Johnson CL: Centers for Dis-
ease Control and Prevention 2000 growth
charts for the United States: improvements to
the 1977 National Center for Health Statistics
version. Pediatrics 2002;109:45–60.
2 Magarey AM, Daniels LA, Boulton TJ: Preva-
lence of overweight and obesity in Australian
children and adolescents: reassessment of
1985 and 1995 data against new standard in-
ternational definitions. Med J Aust 2001;174:
561–564.
3 Lobstein T, Baur L, Uauy R: Obesity in chil-
dren and young people: a crisis in public
health. Obes Rev 2004;5(suppl 1):4–104.
4 Ogden CL, Carroll MD, Kit BK, Flegal KM:
Prevalence of obesity and trends in body mass
index among US children and adolescents,
1999–2010. JAMA 2012;307:483–490.
5 de Onis M, Blossner M, Borghi E: Global
prevalence and trends of overweight and obe-
sity among preschool children. Am J Clin
Nutr 2010;92:1257–1264.
6 Singh AS, Mulder C, Twisk JW, van Mechelen
W, Chinapaw MJ: Tracking of childhood
overweight into adulthood: a systematic re-
view of the literature. Obes Rev 2008; 9: 474–
488.
7 Daniels SR, Arnett DK, Eckel RH, Gidding SS,
Hayman LL, Kumanyika S, Robinson TN,
Scott BJ, St Jeor S, Williams CL: Overweight
in children and adolescents: pathophysiology,
consequences, prevention, and treatment.
Circulation 2005;111:1999–2012.
8 Li J, Motsko SP, Goehring EL Jr, Tave A, Pez-
zullo JC, Jones JK: Prevalence of pediatric dys-
lipidemia: comparison of a population-based
claims database to national surveys. Pharma-
coepidemiol Drug Saf 2010;19:1031–1040.
9 Copeland KC, Zeitler P, Geffner M, Guanda-
lini C, Higgins J, Hirst K, Kaufman FR, Linder
B, Marcovina S, McGuigan P, Pyle L, Tambo-
rlane W, Willi S, TODAY Study Group: Char-
acteristics of adolescents and youth with re-
cent-onset type 2 diabetes: the TODAY co-
hort at baseline. J Clin Endocrinol Metab
2011;96:159–167.
128.111.121.42 - 2/26/2018 3:20:51 AM
Univ. of California Santa Barbara

Age-Related Consequences of Childhood Gerontology 2014;60:222–228 227

Obesity DOI: 10.1159/000356023
Downloaded by:
10 Olshansky SJ, Passaro DJ, Hershow RC,
Layden J, Carnes BA, Brody J, Hayflick L, But-
ler RN, Allison DB, Ludwig DS: A potential
decline in life expectancy in the United States
in the 21st century. N Engl J Med 2005; 352:
1138–1145.
11 Keiller SM, Colley JR, Carpenter RG: Obesity
in schoolchildren and their parents. Ann
Hum Biol 1979;6:443–455.
12 Elks CE, den Hoed M, Zhao JH, Sharp SJ,
Wareham NJ, Loos RJ, Ong KK: Variability in
the heritability of body mass index: a system-
atic review and meta-regression. Front Endo-
crinol (Lausanne) 2012;3:29.
13 Llewellyn CH, Trzaskowski M, Plomin R,
Wardle J: Finding the missing heritability in
pediatric obesity: the contribution of ge-
nome-wide complex trait analysis. Int J Obes
(Lond) 2013;37:1506-1509.
14 Whitaker KL, Jarvis MJ, Beeken RJ, Boniface
D, Wardle J: Comparing maternal and pater-
nal intergenerational transmission of obesity
risk in a large population-based sample. Am J
Clin Nutr 2010;91:1560–1567.
15 Roberts MD, Company JM, Brown JD, To-
edebusch RG, Padilla J, Jenkins NT, Laughlin
MH, Booth FW: Potential clinical translation
of juvenile rodent inactivity models to study
the onset of childhood obesity. Am J Physiol
Regul Integr Comp Physiol 2012; 303:R247–
R258.
16 Jorgensen MJ, Aycock ST, Clarkson TB, Ka-
plan JR: Effects of a Western-type diet on
plasma lipids and other cardiometabolic risk
factors in African green monkeys (Chloroce-
bus aethiops sabaeus). J Am Assoc Lab Anim
Sci 2013;52:448–453.
17 Heerwagen MJ, Miller MR, Barbour LA,
Friedman JE: Maternal obesity and fetal met-
abolic programming: a fertile epigenetic soil.
Am J Physiol Regul Integr Comp Physiol
2010;299:R711–R722.
18 Wisniewski AB, Chernausek SD: Gender in
childhood obesity: family environment, hor-
mones, and genes. Gend Med 2009;6(suppl 1):
76–85.
19 Lerret SM, Garcia-Rodriguez L, Skelton J, Bi-
ank V, Kilway D, Telega G: Predictors of non-
alcoholic steatohepatitis in obese children.
Gastroenterol Nurs 2011;34:434–437.
20 Morrison JA, Friedman LA, Gray-McGuire
C: Metabolic Syndrome in Childhood Pre-
dicts Adult Cardiovascular Disease 25 Years
Later: The Princeton Lipid Research Clinics
Follow-Up Study. Pediatrics 2007; 120: 340–
345.
228 Gerontology 2014;60:222–228
DOI: 10.1159/000356023
21 Juonala M, Magnussen CG, Berenson GS,
Venn A, Burns TL, Sabin MA, Srinivasan SR,
Daniels SR, Davis PH, Chen W, Sun C,
Cheung M, Viikari JS, Dwyer T, Raitakari OT:
Childhood adiposity, adult adiposity, and car-
diovascular risk factors. N Engl J Med 2011;
365:1876–1885.
22 Tirosh A, Shai I, Afek A, Dubnov-Raz G, Aya-
lon N, Gordon B, Derazne E, Tzur D, Shamis
A, Vinker S, Rudich A: Adolescent BMI tra-
jectory and risk of diabetes versus coronary
disease. N Engl J Med 2011;364:1315–1325.
23 Lloyd LJ, Langley-Evans SC, McMullen S:
Childhood obesity and adult cardiovascular
disease risk: a systematic review. Int J Obes
(Lond) 2010;34:18–28.
24 Mattsson N, Rönnemaa T, Juonala M, Viikari
JS, Raitakari OT: Childhood predictors of the
metabolic syndrome in adulthood. The Car-
diovascular Risk in Young Finns Study. Ann
Med 2008;40:542–552.
25 Chen X, Wang Y: Tracking of blood pressure
from childhood to adulthood: a systematic re-
view and meta-regression analysis. Circula-
tion 2008;117:3171–3180.
26 Davis PH, Dawson JD, Riley WA, Lauer RM:
Carotid intimal-medial thickness is related to
cardiovascular risk factors measured from
childhood through middle age: The Musca-
tine Study. Circulation 2001;104:2815–2819.
27 Mahoney LT, Burns TL, Stanford W, Thomp-
son BH, Witt JD, Rost CA, Lauer RM: Coro-
nary risk factors measured in childhood and
young adult life are associated with coronary
artery calcification in young adults: the Mus-
catine Study. J Am Coll Cardiol 1996;27:277–
284.
28 Raitakari OT, Juonala M, Viikari JS: Obesity
in childhood and vascular changes in adult-
hood: insights into the Cardiovascular Risk in
Young Finns Study. Int J Obes (Lond) 2005;
29(suppl 2):S101–S104.
29 Reinehr T, Wunsch R: Intima media thick-
ness-related risk factors in childhood obesity.
Int J Pediatr Obes 2011;6(suppl 1):46–52.
30 Baker JL, Olsen LW, Sorensen TI: Childhood
body-mass index and the risk of coronary
heart disease in adulthood. N Engl J Med
2007;357:2329–2337.
31 Franks PW, Hanson RL, Knowler WC, Siev-
ers ML, Bennett PH, Looker HC: Childhood
obesity, other cardiovascular risk factors, and
premature death. New Engl J Med 2010; 362:
485–493.
32 Berenson GS, Srinivasan SR, Bao W, Newman
WP 3rd, Tracy RE, Wattigney WA: Associa-
tion between multiple cardiovascular risk fac-
tors and atherosclerosis in children and
young adults. The Bogalusa Heart Study. N
Engl J Med 2009;338:1650–1656.
33 Lee JM, Gebremariam A, Vijan S, Gurney JG:
Excess body mass index-years, a measure of
degree and duration of excess weight, and risk
for incident diabetes. Arch Pediatr Adolesc
Med 2012;166:42–48.
34 Morrison JA, Glueck CJ, Horn PS, Wang P:
Childhood predictors of adult type 2 diabetes
at 9- and 26-year follow-ups. Arch Pediatr
Adolesc Med 2010;164:53–60.
35 TODAY Study Group, Zeitler P, Hirst K, Pyle
L, Linder B, Copeland K, Arslanian S, Cuttler
L, Nathan DM, Tollefsen S, Wilfley D,
Kaufman F: A clinical trial to maintain glyce-
mic control in youth with type 2 diabetes. N
Engl J Med 2012;366:2247–2256.
36 Rhodes ET, Prosser LA, Hoerger TJ, Lieu T,
Ludwig DS, Laffel LM: Estimated morbidity
and mortality in adolescents and young adults
diagnosed with Type 2 diabetes mellitus. Dia-
bet Med 2012;29:453–463.
37 Fagherazzi G, Guillas G, Boutron-Ruault MC,
Clavel-Chapelon F, Mesrine S: Body shape
throughout life and the risk for breast cancer
at adulthood in the French E3N cohort. Eur J
Cancer Prev 2013;22:29–37.
38 Hardiman P, Pillay OC, Atiomo W: Polycys-
tic ovary syndrome and endometrial carcino-
ma. Lancet 2003;361:1810–1812.
39 Chromecki TF, Cha EK, Fajkovic H, Rink M,
Ehdaie B, Svatek RS, Karakiewicz PI, Lotan Y,
Tilki D, Bastian PJ, Daneshmand S, Kassouf W,
Durand M, Novara G, Fritsche HM, Burger M,
Izawa JI, Brisuda A, Babjuk M, Pummer K,
Shariat SF: Obesity is associated with worse on-
cological outcomes in patients treated with
radical cystectomy. BJU Int 2013;111:249–255.
40 Calle EE, Thun MJ, Petrelli JM, Rodriguez C,
Heath CW Jr: Body-mass index and mortality
in a prospective cohort of U.S. adults. N Engl
J Med 1999;341:1097–1105.
41 Bibbins-Domingo K, Coxson P, Pletcher MJ,
Lightwood J, Goldman L: Adolescent over-
weight and future adult coronary heart dis-
ease. N Engl J Med 2007;357:2371–2379.
42 Brotman LM, Dawson-McClure S, Huang
KY, Theise R, Kamboukos D, Wang J, Petko-
va E, Ogedegbe G: Early childhood family in-
tervention and long-term obesity prevention
among high-risk minority youth. Pediatrics
2012;129:e621–e628. 128.111.121.42 - 2/26/2018 3:20:51 AM
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