Panagiotakos Demosthenes B, Pitsavos Christos, Yannakoulia Mary, Chrysohoou Christina, Stefanadis Christodoulos
Department of Dietetics and Nutrition, Harokopio University, Athens, Greece.
Atherosclerosis. 2005 Dec;183(2):308-15. doi: 10.1016/j.atherosclerosis.2005.03.010. Epub 2005 Apr 25.
We evaluated the association of obesity with various markers of chronic inflammation, in a population-based sample of 3,042 adults.
During 2001-2002, we randomly enrolled 1,514 men (18-87 years old) and 1,528 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 alpha, 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>or=0.95 in men and>or=0.8 in women, while obesity as body mass index (BMI)>29.9 kg/m(2).
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, alpha 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. R(2)) than the models included BMI, especially in women, even after adjusting for age and various other potential confounders.
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.
在一个基于人群的3042名成年人样本中,我们评估了肥胖与各种慢性炎症标志物之间的关联。
在2001年至2002年期间,我们从希腊阿提卡地区随机招募了1514名男性(18 - 87岁)和1528名女性(18 - 89岁);抽样按该地区的年龄 - 性别分布(2001年人口普查)进行分层。在多个变量中,我们还测量了各种炎症标志物(C反应蛋白、肿瘤坏死因子α、淀粉样蛋白A、白细胞和白细胞介素 - 6)以及人体测量变量(体重、身高、腰围和臀围)。中心性肥胖定义为男性腰臀比≥0.95,女性≥0.8,而肥胖定义为体重指数(BMI)>29.9 kg/m²。
36%的男性和43%的女性存在中心性肥胖(p<0.001),而肥胖分别在20%的男性和15%的女性中存在。与体脂分布正常的参与者相比,中心性肥胖者的C反应蛋白水平高53%,肿瘤坏死因子α水平高30%,淀粉样蛋白A水平高26%,白细胞计数高17%,白细胞介素 - 6水平高42%(所有p<0.05)。我们观察到,在两性中,所有炎症标志物均与BMI(肥胖指标)、腰围以及腰臀比(中心性肥胖指标)相关。此外,即使在调整年龄和其他各种潜在混杂因素后,将腰围或腰臀比作为自变量的模型比包含BMI的模型具有更高的解释能力(即R²),尤其是在女性中。
我们的结果表明,无论年龄和其他潜在混杂因素如何,中心性肥胖与炎症过程之间存在关联。这种关联比总体肥胖与炎症之间的关系更为突出。可以推测,内脏脂肪量的不成比例积累可能通过炎症过程部分地与冠状动脉风险增加相关。