The prevalence of childhood obesity and its consequences are increasing rapidly in low- and middle-income countries (1). It is well documented that childhood obesity tracks into adulthood. Of special concern are the cardiometabolic consequences of obesity, especially hypertension, dyslipidemia, and impaired glucose metabolism, that are already present in young children of different ethnicities (2, 3). It is now established that the origins of the metabolic syndrome trace back to early life (4). Underlying genetic tendency or early-life adverse events may contribute to the metabolic syndrome and its related complications, notably in non-European populations (5). In Iranian children, we found that based on criteria analogous to the Adult Treatment Panel III (6), the metabolic syndrome was present in 14.1% of children 6 to 18 years old (7). Inflammation associated with childhood obesity appears central to the development of insulin resistance and atherosclerosis and may be important in the pathogenesis of other comorbid conditions (8). We have previously documented an increase in serum C-reactive protein (CRP)  and oxidative stress markers in children with abdominal obesity, suggesting that oxidative stress and CRP may be associated with the early inflammatory processes of atherosclerosis (7, 9).