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.
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 childhood 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 comorbidities. However, many factors contribute to average 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.
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 outcomes occur in adults, it is clear that the process of atherosclerosis begins in childhood and is progressive. The Bogalusa and Pathobiological Determinants of Atherosclerosis 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 childhood 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 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 hypertension. Although the mechanism of this relationship is not completely understood, epidemiologic studies consistently show a strong relationship between obesity and hypertension 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.
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.
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 childhood 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 adolescence 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 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 definitions 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.
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. Hepatomegaly 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 completely understood. Clinical studies suggest that insulin resistance may play an important role.32 Children with type 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 intervention for NAFLD. It will be important for other potential interventions to be tested for situations in which weight management cannot be accomplished.
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 ∼33% 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 sleep apnea. The clinical cues to the potential presence of obstructive sleep apnea include a history of snoring, irregular breathing with pauses, and gasping during sleep and daytime somnolence, including school difficulties related to falling 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 due, in part, to the increase in daytime sleepiness. It may also be due to changes in appetite and eating patterns, particularly, eating late in the day and at night.
Obstructive sleep apnea is associated with a variety of cardiovascular abnormalities. Acutely, sleep apnea is associated with hypoxia with an accompanying pulmonary hypertension. On a more chronic basis, obstructive sleep apnea can lead to systemic hypertension, increased right and left ventricular mass, and left ventricular diastolic dysfunction.39 Similarly, an improvement in obstructive sleep apnea, either by substantial weight loss or by other methods, such as continuous positive airway pressure during sleep, can lead to the improvement of blood pressure elevation, LVH and cardiac dysfunction.40
Cross-sectional studies have also shown an association between obesity and asthma in children. Rodriguez et al.41 reported that children with a BMI above the 85th percentile (overweight) had an increased risk of asthma, independent of age, sex, ethnicity, socioeconomic status and exposure to tobacco smoke. It is not clear whether obesity is associated 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 children and adolescents.42
Excess weight can result in excess stress on the musculoskeletal system. In adults, this can result in osteoarthritis, sometimes requiring joint replacement. The most common orthopedic problems in children include tibia vara (Blount's Disease) and slipped capital femoral epiphysis. Both of these orthopedic problems appear to result from the impact of increased weight on a developing skeletal system.
Tibia vera is a mechanical deficiency in the medial tibial growth plate. This causes a bowing of the tibia and an 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 plate, which appears around the age of skeletal maturity. The femur is rotated externally from the growth plate. This can 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 epiphysis appears to include both the mechanical stress of excess weight on developing bone and other biological factors. At this age, the periosteum is thin and is less resistant to shear force caused by bearing increased weight. This abnormality is more common in African American males who are obese. In ∼30% of affected individuals, both legs are involved.43
The development of obesity in childhood and adolescence is associated with psychosocial problems. For example, obese adolescents who seek treatment for their obesity have more symptoms of depression than control subjects without obesity.44 It has not been determined whether the severity of obesity is associated with an increased prevalence of severity of depression. It is also important to note that depression itself may be associated with abnormal eating and exercise patterns, which may contribute to obesity development.45
Another psychosocial outcome of importance is the quality of life. Schwimmer et al.46 found that obese children and adolescents report significantly lower health-related quality of life than peers of normal weight. They also reported that the quality of life for obese children and adolescents was as low as that in children being treated for cancer. Obese children with obstructive sleep apnea reported the lowest quality of life among children and adolescents with obesity.
It is clear that childhood obesity is associated with a wide spectrum of adverse outcomes, including many outcomes that are similar to those seen in adults. Obesity in childhood affects virtually every organ system in an adverse manner. There is still much to be learned about the pathophysiological mechanisms for specific adverse effects of obesity. It will be important for translational research to be done in this area. Such research will inform how to identify patients with obesity who are at high risk for developing specific adverse outcomes. This type of mechanistic research could also inform more specific strategies for treatment of comorbidities when weight management cannot be accomplished or is slower than desirable.
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Conflict of interest
The author has declared no conflict of interest.
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Cite this article
Daniels, S. Complications of obesity in children and adolescents. Int J Obes 33, S60–S65 (2009). https://doi.org/10.1038/ijo.2009.20
- CVD risk factors
- insulin resistance
- nonalcoholic fatty liver disease
- sleep apnea
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