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).
In reviews of the correlates of childhood obesity, discussions of the physical impacts and of the social and emotional impacts are often separate. But this distinction may be artificial. First, although the brain plays a central role in the regulation of energy balance and obesity (Schwartz et al., 2000), it is also the central organ for integrating social stimuli, regulating emotion, and executing social interaction. Not surprisingly, cues that affect both eating and activity behaviors are often social in nature, ranging from sadness to anxiety to boredom.
Social and emotional factors must therefore be recognized not only as potential consequences of obesity but also as potential causes. For example, depressed mood in children and adolescents may precede the development of obesity and not just follow it (Pine et al., 2001; Goodman and Whitaker,