International Journal of Obesity (2009) 33, S60–S65

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REVIEW
Complications of obesity in children and adolescents
SR Daniels

Department of Pediatrics, University of Colorado School of Medicine, and The Children’s Hospital, Denver, CO, USA

The increasing prevalence and severity of obesity in children and adolescents has provided greater emphasis on the wide variety
of comorbid conditions and complications that can be experienced as a consequence of obesity. These complications can occur
both in the short term and in the long term. Some complications, earlier thought to be long-term issues, which would only
occur in adulthood, have now been shown to occur in children and adolescents. These findings have raised concerns about the
overall health experience of those who develop obesity early in life and have even raised questions about whether the obesity
epidemic might shorten the life span of the current generation of children. In this paper, I will examine current knowledge
regarding the different organ systems that may be impacted by childhood obesity.
International Journal of Obesity (2009) 33, S60–S65; doi:10.1038/ijo.2009.20

Keywords: mortality; CVD risk factors; insulin resistance; dyslipidemia; nonalcoholic fatty liver disease; sleep apnea

Mortality comorbidities. However, many factors contribute to average

It has been recognized for some time that obesity results in
increased risk for mortality. The Metropolitan Life Insurance
Company’s relative weight scale has been in use for decades.1
Although this recognizes the potential impact of obesity on
the risk of mortality, it does not provide useful information
on whether obesity developed at an earlier age will be
associated with a greater mortality risk compared with that
developed at an older age.
It can also be difficult to establish the independence
obesity may have as a risk factor for mortality compared with
other factors, some of which may, in part, be related to
obesity. Mokdad et al.2 attempted to discern the number of
deaths attributable to obesity. The initial estimate was
400 000 annually in the United States, which was similar to
the number of deaths attributable to cigarette smoking.
However, these findings and the methodology used to
generate them have been called into question. A subsequent
analysis estimated annual mortality due to obesity at
112 000.3 However, it is clear from all of these analyses that
the relative toll of obesity is high.
Olshansky et al.4 evaluated the potential effect of child-
hood obesity on life span. Over the past century, there has
been a trend toward increasing life span over time. Their
analysis predicts a shorter life span for the current generation
of children in large part because of obesity and its related
Correspondence: Dr SR Daniels, Department of Pediatrics, University of
Colorado at Denver and Health Science Center, 13123 E. 16th Avenue, B065,
Aurora, CO 80045, USA.
E-mail: daniels.stephen@tchden.org
life span and medical science continues to provide new
diagnostic and treatment approaches for acute and chronic
diseases.
The various medical complications of obesity in childhood
are presented in Table 1. It can be seen that those
complications affect a variety of organ systems.
Cardiovascular disease
The Framingham study has documented a connection
between obesity and the development of cardiovascular
disease (CVD) in adults.5 Similarly, in the Nurses Health
Study, obesity is associated with increased risk of both non-
fatal and fatal myocardial infarction.6 Although these out-
comes occur in adults, it is clear that the process of
atherosclerosis begins in childhood and is progressive. The
Bogalusa and Pathobiological Determinants of Atherosclero-
sis in Youth pathology studies have shown a strong
association between overweight and the increased presence
of atherosclerotic lesions in both the aorta and coronary
arteries7–8 in young individuals. Mahoney et al.9 used
computed tomography to evaluate young adults in the
Muscatine Study who had CVD risk factors measured as
children. They found that increased weight during child-
hood was the strongest predictor of coronary calcium later in
life. Coronary calcium has been shown to be a marker for
plaque formation in the coronary arteries and is associated
with increased risk of myocardial infarction. Gidding et al.10
evaluated the presence of coronary calcium in adolescents

Table 1 Disorders related to childhood obesity
System and disorder
Cardiovascular
Hypertension
Left ventricular hypertrophy
Atherosclerosis
Metabolic
Insulin resistance
Dyslipidemia
Metabolic syndrome
Type 2 diabetes
Pulmonary
Asthma
Obstructive sleep apnea
Gastrointestinal
Nonalcoholic fatty liver disease
Gastroesohageal reflux
Skeletal
Tibia vara (Blount disease)
Slipped capital-femoral epiphysis
Other
Polycystic ovary syndrome
Pseudotumor cerebri
Comorbid conditions of childhood obesity are presented by organ systems.
with familial hypercholesterolemia. They found that in these
high-risk individuals, coronary calcium can be present early
in life. They also found that in the presence of high low-
density lipoprotein cholesterol, a high body mass index
(BMI) was an important factor in determining the presence
of calcified coronary lesions.
Obesity is quite important in the pathogenesis of hyper-
tension. Although the mechanism of this relationship is not
completely understood, epidemiologic studies consistently
show a strong relationship between obesity and hyperten-
sion for both adults and children.11 Rosner et al.12 have
shown that the relative risk of hypertension associated
with overweight ranges from 2.5 to 3.7 in children and
adolescents.
Evaluation of national survey data has shown that there
has been a trend of increasing blood pressure that has
paralleled the increase in the prevalence of obesity.13
Investigators of the Muscatine Study have shown that in
addition to the childhood level of blood pressure, the
development of overweight in childhood is one of the
strongest predictors of the level of blood pressure in
adulthood.14 More recently, Din-Dzietham et al.15 have
evaluated national survey data in the United States from
1963 to 2002 for 8- to 17-year-old children and adolescents.
They found that the prevalence of both pre-high blood
pressure and high blood pressure increased by 2.3 and 1%,
respectively, between 1988 and 1999. This reversed an earlier
downward trend. This increase in the prevalence of high
blood pressure was at least partly explained by increased
obesity and in particular an increase in abdominal obesity.
Complications of obesity in childhood
SR Daniels
S61
Left ventricular hypertrophy (LVH) has been shown to be
an independent risk factor for the development of CVD
morbidity and mortality in adults.16 Studies have shown that
a number of factors, including obesity and blood pressure
elevation, are associated with increased left ventricular mass.
Yoshinaga et al.17 have shown that young individuals with
obesity have, on average, greater left ventricular mass.
Daniels et al.18 have shown that among children and
adolescents with hypertension, an increased BMI is
associated with more severely increased left ventricular mass
index, with some individuals with hypertension even
reaching a point where their LVH would be associated with
a four-fold increase in risk in cardiovascular end points.
Flynn and Alderman19 reported a prevalence of LVH of 30%
in obese children with hypertension compared with 18% in
non-obese children with hypertension.
Metabolic
Obesity is associated with a wide array of metabolic
complications in adults. These include insulin resistance,
dyslipidemia and type 2 diabetes mellitus. These metabolic
complications have now also been found to be associated
with obesity in adolescents.
Steinberger et al.20 have shown that obesity during child-
hood is associated with decreased insulin sensitivity and
increased circulating insulin levels. They have also shown
that these abnormalities often persist into young adulthood.
Insulin resistance is an important factor in the development
of type 2 diabetes. The period of growth and development
during adolescence is associated with a normal increase in
insulin resistance.21 If additional insulin resistance develops
related to obesity during this time, then it may lead first to
glucose intolerance, and then to type 2 diabetes mellitus.
The prevalence of type 2 diabetes has increased in adoles-
cence and has been reported in children as young as 8 years
of age.22 Although the classification of type 1 and type 2
diabetes is complex in obese adolescents, a review from the
American Diabetes Association reports that as high a
proportion as 45% of newly diagnosed cases of diabetes in
children and adolescents are now type 2 diabetes in the era
of increased prevalence and severity of obesity in young
individuals.23
Dyslipidemia may occur in children and adolescents as a
result of obesity. The most common abnormality of lipids
and lipoproteins associated with obesity is an increase in
triglycerides and a decrease in high-density lipoprotein
cholesterol. This has been called atherogenic dyslipidemia
because of its potential to accelerate atherosclerosis. Obesity
can also contribute to an increase in low-density lipoprotein
cholesterol. However, it is unclear if this is a direct effect or
related to increased levels of saturated fat and cholesterol
often present in the diet of overweight individuals during
childhood. In the Muscatine Study, BMI and the change in
International Journal of Obesity
 Complications of obesity in childhood
SR Daniels
S62
BMI over time were strong predictors of adult lipid and
lipoprotein levels.24 This is almost certainly an important
factor in explaining the observation that weight during
childhood is a predictor of coronary artery calcium in young
adulthood.9
The Adult Treatment Panel III of the National Cholesterol
Education Program defined a clinical entity known as the
Metabolic Syndrome. This constellation of risk factors,
including elevated blood pressure, increased triglycerides
and low high-density lipoprotein cholesterol, has been
shown to cluster in individuals who are obese, particularly
those with central or abdominal adiposity.25 The Metabolic
Syndrome has been shown to be associated with an increased
risk of CVD and type 2 diabetes in adults.26 Presently, there is
no clear definition of the Metabolic Syndrome in children or
adolescents. A number of potential definitions have been
proposed primarily by taking the adult factors for Metabolic
Syndrome and then constructing percentile-based defini-
tions for children. The difficulty is that there is not an
outcome-based method to establish the optimum variables
or cut points for children. On the one hand, it does appear
that factor analyses show similar clustering of risk factors in
children as compared with adults27 and on the other, it also
appears that adolescents have substantial variability in
whether they meet the definition of metabolic syndrome
or not over time.28 This lack of consistency or stability of the
diagnosis suggests that the diagnosis of Metabolic Syndrome
may be less useful in adolescence compared with that in
adulthood. Nevertheless, studies of populations have shown
that the prevalence of Metabolic Syndrome in obese children
and adolescents may be as high as 30%.29 Weiss et al.30 have
shown that for each one-half unit increase in the BMI Z-
score, there is approximately a 50% increase in the risk of the
metabolic syndrome in overweight children and adolescents.
Gastrointestinal
A major concern is the development on nonalcoholic fatty
liver disease (NAFLD). This disorder is characterized by the
accumulation of macrovesicular fat in hepatocytes. This
condition was first recognized in adults in the 1950s. The
first reports of NAFLD in children were in the 1980s.31
NAFLD can be progressive. Patients can develop non-
alcoholic steatohepatitis (NASH) with an inflammatory
component that can then progress to hepatic fibrosis and
ultimately cirrhosis. Adult patients have even required liver
transplantation as a result of the progression of NAFLD.
Children with NAFLD are usually asymptomatic. Hepato-
megaly is reported to be present in 40–50% of children with
NAFLD; however, this may be difficult to discern on physical
examination of an obese child or adolescent.32
The pathophysiology of NAFLD and NASH is not com-
pletely understood. Clinical studies suggest that insulin
resistance may play an important role.32 Children with type
International Journal of Obesity
2 diabetes mellitus are prone to develop NAFLD. As high a
proportion as 50% of such patients are suspected to have a
fatty liver at the time of diagnosis.33
The prevalence of fatty liver in children is not precisely
known. This is difficult to determine, in part, because liver
biopsy presents the most definitive diagnosis. A recent
autopsy-based study in southern California evaluated
fatty liver in children and adolescents age 2–19 years.34
Schwimmer et al.34 reported a prevalence of fatty liver of
9.6% in this age group with a 95% confidence interval of
7.4–11.4%. In this study, most children had fatty liver alone,
with only 25% of affected children having NASH and only
3% having advanced fibrosis. On the other hand, referral
studies have shown a prevalence of NASH of 68% and a
prevalence of fibrosis of 8% with liver biopsy.35
Obesity is the most important risk factor for development
of NAFLD and NASH. In addition, Hispanic children appear
to be at higher risk than white or black children.36 Presently,
weight management is the most important clinical inter-
vention for NAFLD. It will be important for other potential
interventions to be tested for situations in which weight
management cannot be accomplished.
Pulmonary
Obesity and obstructive sleep apnea are closely related in
adults and children. The relationships among obesity,
obstructive sleep apnea, and cardiovascular and other
abnormalities are depicted in Figure 1. Mallory et al.37 found
that B33% of severely overweight children had symptoms
associated with obstructive sleep apnea, whereas 5% had
severe obstructive sleep apnea. Both acute and chronic
cardiovascular outcomes are associated with obstructive
Obesity
Pharyngeal and
submental fat Abdominal fat
Chest-wall fat
Upper airway Lung volume
collapsability
Obstructive
sleep apnea
Hypoxemia
Cardiovascular
abnormality
Figure 1 Relationship of obesity to obstructive sleep apnea and cardiovas-
cular disease.
 Complications of obesity in childhood
SR Daniels
S63
sleep apnea. The clinical cues to the potential presence of to shear force caused by bearing increased weight. This
obstructive sleep apnea include a history of snoring, irregular abnormality is more common in African American males
breathing with pauses, and gasping during sleep and daytime who are obese. In B30% of affected individuals, both legs are
somnolence, including school difficulties related to falling involved.43
asleep during class or behavioral issues during class.38
Obstructive sleep apnea may also contribute to ongoing
weight gain and increasing severity of obesity. This may be
Psychosocial
due, in part, to the increase in daytime sleepiness. It may also
be due to changes in appetite and eating patterns, particu-
The development of obesity in childhood and adolescence is
larly, eating late in the day and at night.
associated with psychosocial problems. For example, obese
Obstructive sleep apnea is associated with a variety of
adolescents who seek treatment for their obesity have more
cardiovascular abnormalities. Acutely, sleep apnea is asso-
symptoms of depression than control subjects without
ciated with hypoxia with an accompanying pulmonary
obesity.44 It has not been determined whether the severity
hypertension. On a more chronic basis, obstructive sleep
of obesity is associated with an increased prevalence of
apnea can lead to systemic hypertension, increased right and
severity of depression. It is also important to note
left ventricular mass, and left ventricular diastolic dysfunc-
that depression itself may be associated with abnormal
tion.39 Similarly, an improvement in obstructive sleep apnea,
eating and exercise patterns, which may contribute to
either by substantial weight loss or by other methods, such
obesity development.45
as continuous positive airway pressure during sleep, can lead
Another psychosocial outcome of importance is the
to the improvement of blood pressure elevation, LVH and
quality of life. Schwimmer et al.46 found that obese children
cardiac dysfunction.40
and adolescents report significantly lower health-related
Cross-sectional studies have also shown an association
quality of life than peers of normal weight. They also
between obesity and asthma in children. Rodriguez et al.41
reported that the quality of life for obese children and
reported that children with a BMI above the 85th percentile
adolescents was as low as that in children being treated for
(overweight) had an increased risk of asthma, independent
cancer. Obese children with obstructive sleep apnea reported
of age, sex, ethnicity, socioeconomic status and exposure to
the lowest quality of life among children and adolescents
tobacco smoke. It is not clear whether obesity is associated
with obesity.
with the pathophysiology of asthma or whether it is a factor
that makes asthma more severe when it is already present. In
adults, weight loss can result in the improvement of
pulmonary function. It is not clear if that also occurs in Conclusion
children and adolescents.42
It is clear that childhood obesity is associated with a wide
spectrum of adverse outcomes, including many outcomes
Orthopedic that are similar to those seen in adults. Obesity in childhood
affects virtually every organ system in an adverse manner.
Excess weight can result in excess stress on the musculoske- There is still much to be learned about the pathophysio-
letal system. In adults, this can result in osteoarthritis, logical mechanisms for specific adverse effects of obesity. It
sometimes requiring joint replacement. The most common will be important for translational research to be done in this
orthopedic problems in children include tibia vara (Blount’s area. Such research will inform how to identify patients with
Disease) and slipped capital femoral epiphysis. Both of these obesity who are at high risk for developing specific adverse
orthopedic problems appear to result from the impact of outcomes. This type of mechanistic research could also
increased weight on a developing skeletal system. inform more specific strategies for treatment of comorbid-
Tibia vera is a mechanical deficiency in the medial tibial ities when weight management cannot be accomplished or is
growth plate. This causes a bowing of the tibia and an slower than desirable.
abnormal gait. This occurs most commonly in boys over the
age of 9 years who are substantially overweight.
Slipped capital femoral epiphysis is a disorder of growth Conflict of interest
plate, which appears around the age of skeletal maturity. The
femur is rotated externally from the growth plate. This can The author has declared no conflict of interest.
cause hip and/or knee pain and make it difficult to walk. This
lesion requires a surgical repair to allow the patient to
ambulate. The pathophysiology of slipped capital femoral References
epiphysis appears to include both the mechanical stress of
excess weight on developing bone and other biological 1 Metropolitan Life Insurance Company. New weight standards for
factors. At this age, the periosteum is thin and is less resistant men and women. Stat Bull 1959; 40: 1–4.

International Journal of Obesity

 Complications of obesity in childhood
SR Daniels
S64
2 Mokdad AH, Marks JS, Stoup DF, Gerberding JL. Actual causes of
death in the United States, 2000. JAMA 2005; 293: 293–294.
3 Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific
excess deaths associated with underweight, overweight, and
obesity. JAMA 2007; 298: 2028–2037.
4 Olshansky SJ, Passaro DJ, Hershow RC, Layden J, Carnes BA,
Brody J et al. A potential decline in life expectancy in the
United States in the 21st century. N Engl J Med 2005; 352:
1138–1145.
5 Ingelsson E, Sullivan LM, Fox CS, Murabito JM, Benjamin EJ,
Polak JF et al. Burden and prognostic importance of subclinical
cardiovascular disease in overweight and obese individuals.
Circulation 2007; 116: 375–384.
6 Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B,
Monson RR et al. A prospective study of obesity and risk
of coronary heart disease in women. N Engl J Med 1990; 322:
882–889.
7 Berenson GS, Srinivasan SR, Bao W, Newman III WP, Tracy Re,
Wattigney WA. Association between multiple cardiovascular risk
factors and atherosclerosis in children and young adults. The
Bogalusa Heart Study. N Engl J Med 1998; 338: 1650–1656.
8 McGill Jr HC, McMahan CA, Zieske AW, Malcom GT, Tracy RE,
Strong JP. Effects of nonlipid risk factors on atherosclerosis in
youth with a favorable lipoprotein profile. Circulation 2001; 103:
1546–1550.
9 Mahoney LT, Burns TL, Stanford W, Thompson BH, Witt JD,
Rost CA et al. Coronary risk factors measured in childhood and
young adult life are associated with coronary artery calcification
in young adults: the Muscatine Study. J Am Coll Cardiol 1996; 27:
277–284.
10 Gidding SS, Bookstein LC, Chomka EV. Usefulness of electron
beam tomography in adolescents and young adults with
heterozygous familial hypercholesterolemia. Circulation 1998;
98: 2580–2583.
11 Sorof J, Daniels S. Obesity hypertension in children: a problem of
epidemic proportions. Hypertension 2002; 40: 441–4417.
12 Rosner B, Prineas R, Daniels SR, Loggie J. Blood pressure
differences between blacks and whites in relation to body size
among US children and adolescents. Am J Epidemiol 2000; 151:
1007–1019.
13 Muntner P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in
blood pressure among children and adolescents. JAMA 2004; 291:
2107–2113.
14 Lauer RM, Clarke WR. Childhood risk factors for high
adult blood pressure: the Muscatine Study. Pediatrics 1989; 84:
633–641.
15 Din-Dzietham R, Liu Y, Bielo MV, Shamsa F. High blood pressure
trends in children and adolescents in national surveys, 1963 to
2002. Circulation 2007; 116: 1488–1496.
16 de Simone G, Devereur RB, Daniels SR, Koren MJ, Meyer RA,
Laragh JH. Effect of growth on variability of left ventricular mass:
assessment of allometric signals in adults and children and their
capacity to predict cardiovascular risk. J Am Coll Cardiol 1995; 25:
1056–1062.
17 Yoshinaga M, Yuasa Y, Hatano H, Kono Y, Nomure Y, Oku S et al.
Effect of total adipose weight and systemic hypertension on left
ventricular mass in children. Am J Cardiol 1995; 76: 785–787.
18 Daniels SR, Loggie JM, Khoury P, Kimball TR. Left ventricular
geometry and severe left ventricular hypertrophy in children and
adolescents with essential hypertension. Circulation 1998; 97:
1907–1911.
19 Flynn JT, Alderman MH. Characteristics of children with primary
hypertension seen at a referral center. Pediatr Nephrol 2005; 20:
961–966.
20 Steinberger J, Moran A, Hong CP, Jacobs Jr DR, Sinaiko AR.
Adiposity in childhood predicts obesity and insulin resistance in
young adulthood. J Pediatr 2001; 138: 469–473.
21 Ball GD, Huang TT, Gower BA, Cruz ML, Shaibi GO, Weigensberg
MJ et al. Longitudinal changes in insulin sensitivity, insulin
International Journal of Obesity
secretion, and beta-cell function during puberty. J Pediatr 2006;
148: 16–22.
22 Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D,
Khoury PR, Zeitler P. Increased incidence of non-insulin-depen-
dent diabetes mellitus among adolescents. J Pediatr 1996; 128:
608–615.
23 American Diabetes Association. Type 2 diabetes in children and
adolescents. Diabetes Care 2000; 23: 381–389.
24 Lauer RM, Lee J, Clarke WR. Factors affecting the relationship
between childhood and adult cholesterol levels: the Muscatine
Study. Pediatrics 1988; 82: 309–318.
25 National Cholesterol Education Program (NCEP) Expert Panel on
Detection, Evaluation, Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III). Third Report of the National
Cholesterol Education Program (NCEP) Expert Panel on Detec-
tion, Evaluation, and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III) final report. Circulation 2002;
106: 3143–3421.
26 American Heart Association; National Heart, Lung, and Blood
Institute, Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel
RH, Franklin BA et al. Diagnosis and management of the
metabolic syndrome. An American Heart Association/National
Heart, Lung, and Blood Institute Scientific Statement. Executive
summary. Cardiol Rev 2005; 13: 322–327.
27 Goodman E, Dolan LM, Morrison JA, Daniels SR. Factor analysis
of clustered cardiovascular risks in adolescence: obesity is the
predominant correlate of risk among youth. Circulation 2005;
111: 1970–1977.
28 Goodman E, Daniels SR, Meigs JB, Dolan LM. Instability in the
diagnosis of metabolic syndrome in adolescents. Circulation 2007;
115: 2316–2322.
29 Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH.
Prevalence of a metabolic syndrome phenotype in adolescents:
findings from the third National Health and Nutrition
Examination Survey, 1988–1994. Arch Pediatr Adolesc Med 2003;
157: 821–827.
30 Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE,
Yeckel CW et al. Obesity and the metabolic syndrome in children
and adolescents. N Engl J Med 2004; 350: 2362–2374.
31 Moran JR, Ghishan FK, Halter SA, Green HL. Steatohepatitis in
obese children: a cause of chronic liver dysfunction. Am J
Gastroenterol 1983; 78: 372–377.
32 Schwimmer JB, Deutsch R, Rauch JB, Behling C, Newbury R,
Lavine JE. Obesity, insulin resistance, and other clinicopatho-
logical correlates of pediatric nonalcoholic fatty liver disease.
J Pediatr 2003; 143: 500–505.
33 Nadeau KJ, Klingensmith G, Zeitler P. Type 2 diabetes in children
is frequently associated with elevated alanine aminotransferase.
J Pediatr Gastroenterol Nutr 2005; 41: 94–98.
34 Schwimmer JB, Deutsch R, Kahen T, Lavine JE, Stanley C, Behling
C. Prevalence of fatty liver in children and adolescents. Pediatrics
2006; 118: 1388–1393.
35 Schwimmer JB, Behling C, Newbury R, Deutsch R, Nievergelt C,
Schork NJ et al. Histopathology of pediatric nonalcoholic fatty
liver disease. Hepatology 2005; 42: 641–649.
36 Schwimmer JB, McGreal N, Deutsch R, Finegold M, Lavine JE. The
influence of gender, race, and ethnicity on suspected fatty liver in
obese adolescents. Pediatrics 2005; 115: e561–e565.
37 Mallory Jr GB, Fiser DH, Jackson R. Sleep-associated breathing
disorders in morbidly obese children and adolescents. J Pediatr
1989; 115: 892–897.
38 Rhodes SK, Shimoda KC, Waid LR, O’Neil PM, Oexmann MJ,
Collop NA et al. Neurocognitive deficits in morbidly
obese children with obstructive sleep apnea. J Pediatr 1995; 127:
741–744.
39 Amin RS, Kimball TR, Bean JA, Jeffries JL, Wilging JP, Cotton RT
et al. Left ventricular hypertrophy and abnormal ventricular
geometry in children and adolescents with obstructive sleep
apnea. Am J Respir Crit Care Med 2002; 165: 1395–1399.

40 Amin RS, Kimball TR, Kalra M, Jeffries JL, Carroll JL, Bean JA et al.
Left ventricular function in children with sleep-disordered
breathing. Am J Cardiol 2005; 95: 801–804.
41 Rodriguez MA, Winkleby MA, Ahn D, Sundquist J,
Kraemer HC. Identification of population subgroups of
children and adolescents with high asthma prevalence:
findings from the Third National Health and Nutrition
Examination Survey. Arch Pediatr Adolesc Med 2002; 156:
269–275.
42 Stenius-Aarniala B, Poussa T, Kvarnstrom J, Gronlund EL,
Ylikahri M, Mustajoki P. Immediate and long term effects of
weight reduction in obese people with asthma: randomised
controled study. BMJ 2000; 320: 827–832. Erratum in BMJ 2000;
320: 984.
Complications of obesity in childhood
SR Daniels
S65
43 Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronson DD.
Acute slipped capital femoral epiphysis: the importance of
physical stability. J Bone Joint Surg Am 1993; 75: 1134–1140.
44 Britz B, Siegfried W, Ziegler A, Lamertz C, Herpertz-Dahlmann
BM, Remschmidt H et al. Rates of psychiatric disorders in a
clinical study group of adolescents with extreme obesity and in
obese adolescents ascertained via a population based study. Int J
Obes Relat Metab Disord 2000; 24: 1707–1714.
45 Pine DS, Goldstein RB, Wolk S, Weissman MM. The association
between childhood depression and adulthood body mass index.
Pediatrics 2001; 107: 1049–1056.
46 Schwimmer JS, Burwinkle TM, Varni JW. Health-related quality of
life of severely obese children and adolescents. JAMA 2003; 289:
1813–1819.
International Journal of Obesity