Several thorough reviews (Dietz, 1998a,b; Must and Strauss, 1999; Deckelbaum and Williams, 2001; Styne, 2001; Must and Anderson, 2003) have found childhood obesity to be associated with a wide array of disorders that affect multiple organ systems. These disorders include hypertension, dyslipidemia, glucose intolerance/insulin resistance, hepatic steatosis, cholelithiasis, sleep apnea, menstrual abnormalities, impaired balance, and orthopedic problems. Some of these conditions produce clinical symptoms in obese children, while others do not; however, the metabolic and physiologic changes associated with childhood obesity, along with the obesity itself, tend to track into adult life and eventually enhance the risks of disease, disability, and death.
In 2000, it was estimated that 400,000 deaths were attributed to poor diet and physical inactivity in the United States (Mokdad et al., 2004), an increase of one-third from 300,000 annual deaths attributed to diet and sedentary activities in 1990 (McGinnis and Foege, 1993). Although these risk factors represent the second leading cause of deaths among Americans, diet and physical inactivity are predicted to exceed tobacco as the leading cause of deaths in the future (Mokdad et al., 2004).
Of the multiple health correlates of the childhood obesity epidemic, perhaps the one that has received greatest attention is the increased prevalence of type 2 diabetes in children.5 By one population-based estimate from southwestern Ohio, a ten-fold increase in the prevalence of type 2 diabetes in children between 1982 and 1994 accounted for one-third of all new cases of diabetes (including type 1 and type 2) in children by 1994 (Pinhas-Hamiel et al., 1996). For individuals born in the United States in 2000, the lifetime risk of being diagnosed with diabetes at some point in their lives is estimated at 30 percent for boys and 40 percent for girls if
5Type 2 diabetes was previously referred to as adult-onset diabetes and type 1 diabetes was previously called juvenile-onset diabetes.
obesity rates level off (Narayan et al., 2003). Nearly all children with type 2 diabetes are obese, and a disproportionate number are Native American, African American, Hispanic, or Asian/Pacific Islander (Fagot-Campagna et al., 2000; Goran et al., 2003; Davis et al., 2004).
Several risk factors—including increased body fat (especially abdominal fat), insulin resistance, ethnicity, and the onset of puberty—have been identified as contributors to the development of type 2 diabetes, and they appear to have an additive influence (Goran et al., 2003). Accurate estimates of the prevalence of diabetes in U.S. children are difficult to determine. It has been estimated that the prevalence of diabetes is 0.41 percent in U.S. youth aged 12-19 years (approximately 100,000 U.S. adolescents) and the prevalence of impaired fasting glucose is 1.76 percent (approximately 500,000 U.S. adolescents) (Fagot-Campagna et al., 2001). Better estimates for children are not possible because the prevalence of type 2 diabetes in this population is still relatively low. NHANES is the only current national data collection effort that could potentially make such an estimate. However, the sample sizes from NHANES are not large enough to make a stable point estimate of the prevalence.
The childhood obesity epidemic may result in increased risk of type 2 diabetes. One study found that for each adolescent diagnosed with type 2 diabetes, there are 5 others with impaired fasting glucose, an indicator of insulin resistance below the diagnostic threshold for type 2 diabetes (Fagot-Campagna et al., 2001). Furthermore, the degree of insulin resistance in children increases with the severity of body fatness, as it does in adults (ADA, 2000). Thus, the combination of more obese children and the increased severity of obesity suggests that larger numbers of children will reach the diagnostic threshold for type 2 diabetes. Finally, it is estimated that approximately three-fourths of obese adolescents will be overweight as young adults (Guo et al., 2002) and will likely face the persistent risk of developing type 2 diabetes.
The increased prevalence of obesity among adults of all ages also has been associated with a similar increase in the prevalence of diabetes (Mokdad et al., 2001). In fact, the increase in diabetes prevalence has been greatest in young adults aged 30 to 39 years, with prevalence almost doubling between 1990 and 2001 (Mokdad et al., 2000, 2003). Moreover, the development of all of the major complications of diabetes, including retin-opathy, nephropathy, and neuropathy, are related to duration of disease. Those who develop diabetes earlier in life generally will develop costly complications earlier with the potential for premature mortality. For example, among 79 individuals in a Canadian referral clinic who were diagnosed with type 2 diabetes before the age of 17 and who were followed up from ages 18 to 33 years, two had died suddenly while on dialysis and three more were currently receiving dialysis (Dean and Flett, 2002).
A potentially even more important complication of childhood obesity may be the metabolic syndrome, diagnosed when a person has at least three of five metabolic abnormalities: glucose intolerance, abdominal obesity, hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and high blood pressure (NHLBI, 2002). The metabolic syndrome is now present in approximately one-quarter of all U.S. adults (Ford et al., 2002; Park et al., 2003) and in nearly 30 percent of U.S. children and youth who are obese (Cook et al., 2003).
Among adults, the metabolic syndrome is associated not only with type 2 diabetes (Haffner et al., 1992; Cook et al., 2003) but also with cardiovascular disease (Isomaa et al., 2001; Cook et al., 2003) and a higher mortality rate (Lakka et al., 2002; Cook et al., 2003). Even among those obese youth who do not yet have clinical diabetes, components of the metabolic syndrome appear to contribute to the development of atherosclerosis (Mahoney et al., 1996; Berenson et al., 1998; McGill et al., 2002). Ultimately, it may be the association of childhood obesity with the metabolic syndrome, rather than exclusively with diabetes, that may comprise the greatest physical health threat of childhood obesity.
It is possible that if the childhood obesity epidemic continues at its current rate, conditions related to type 2 diabetes—such as blindness, amputation, coronary artery disease, stroke, and kidney failure—will become ordinary in middle-aged people. Additionally, risk factors for cancer in obese adults, such as hormone alterations, may be present in obese children and contribute to a higher incidence of certain types of cancer later in life (Gascon et al., 2004). Thus, these conditions may affect a greater proportion of the population than current morbidity. This is a serious prospect given that obesity accounts for a level of morbidity comparable to that of smoking and poverty (Sturm and Wells, 2001).
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