The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study

Objective We evaluated the association of obesity with various markers of chronic inflammation, in a population-based sample of 3042 adults. Methods During 2001–2002, we randomly enrolled 1514 men (18–87 years old) and 1528 women (18–89 years old), from the Attica area, Greece; the sampling was stratified by the age–sex distribution of the region (census 2001). Among several variables, we also measured various inflammatory markers (C-reactive protein, tumor necrosis factor α, amyloid A, white blood cells and interleukin-6) and anthropometric variables (weight, height, waist and hip circumferences). Central fat was defined as waist-to-hip ratio ≥ 0.95 in men and ≥ 0.8 in women, while obesity as body mass index (BMI) > 29.9 kg/m2. Results Central fat prevailed in 36% of men and 43% of women (p < 0.001), while obesity prevailed in 20% of men and 15% of women, respectively. Compared to participants with normal body fat distribution, those with central fat exhibited 53% higher C-reactive protein levels, 30% higher tumor necrosis factor, α levels, 26% higher amyloid A levels, 17% higher white blood cell counts and 42% higher interleukin-6 levels (all p < 0.05). We observed that all inflammation markers were related to BMI (index for obesity), waist and to waist-to-hip ratio (indices for central fat), in both genders. Moreover, the models that included waist or waist-to-hip ratio as independent variable had higher explanatory ability (i.e. R2) than the models included BMI, especially in women, even after adjusting for age and various other potential confounders. Conclusion Our results suggest a relationship between central adiposity and inflammation process, irrespective of age and other potential confounders. This association was more prominent than the relationship between total obesity and inflammation. It could be hypothesized that a disproportionate accumulation of visceral fat mass could be partially associated with increased coronary risk, through inflammation process.