Moore Lynn L, Chadid Susan, Singer Martha R, Kreger Bernard E, Denis Gerald V
Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, Massachusetts.
Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Cancer Epidemiol Biomarkers Prev. 2014 Oct;23(10):2057-65. doi: 10.1158/1055-9965.EPI-14-0240. Epub 2014 Jul 10.
It is unknown whether the risk for obesity-related cancers differs between metabolically unhealthy and healthy overweight/obese adults.
Data on body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), and random blood glucose in Framingham Heart Study adults (n = 3,763) ages 55 to 69 years were used to estimate risks of obesity-related cancers (n = 385), including postmenopausal breast, female reproductive, colon, liver, gallbladder, pancreas, and kidney cancers, as well as esophageal adenocarcinomas. Multivariable-adjusted Cox proportional hazards models were used to estimate risk for obesity-related cancers associated with body fat and metabolic health (as defined by glucose levels) among subjects in three risk groups (vs. referent group with normal weight/normal glucose): normal weight/elevated glucose, overweight/normal glucose, and overweight/elevated glucose.
Overweight adults [BMI ≥ 25 or WHtR ≥ 0.51 (men) and ≥0.57 (women)] with elevated glucose (≥125 mg/dL) had a statistically significant 2-fold increased risk of developing obesity-related cancer, whereas overweight adults with normal glucose had a 50% increased risk. Normal-weight adults with elevated glucose had no excess cancer risk. The effects of BMI and WHtR were independent of one another. Finally, overweight women with elevated blood glucose had a 2.6-fold increased risk [95% confidence interval (CI), 1.4-4.9] of female reproductive (cervical, endometrial, uterine cancers) and postmenopausal breast cancers, whereas overweight women with normal glucose levels had only a 70% increased risk (95% CI, 1.1-2.5).
These results suggest that cancer risk may be lower among metabolically healthy overweight/obese older adults than among overweight/obese adults with metabolic dysfunction.
Metabolic dysfunction and obesity act synergistically to increase cancer risk.
代谢不健康的超重/肥胖成年人与健康的超重/肥胖成年人相比,患肥胖相关癌症的风险是否存在差异尚不清楚。
利用弗雷明汉心脏研究中55至69岁成年人(n = 3763)的体重指数(BMI)、腰围(WC)、腰高比(WHtR)和随机血糖数据,估计肥胖相关癌症(n = 385)的风险,包括绝经后乳腺癌、女性生殖系统癌症、结肠癌、肝癌、胆囊癌、胰腺癌、肾癌以及食管腺癌。多变量调整的Cox比例风险模型用于估计三个风险组(与体重正常/血糖正常的参照组相比)中与体脂和代谢健康(由血糖水平定义)相关的肥胖相关癌症风险:体重正常/血糖升高、超重/血糖正常、超重/血糖升高。
血糖升高(≥125 mg/dL)的超重成年人[BMI≥25或WHtR≥0.51(男性)且≥0.57(女性)]患肥胖相关癌症的风险在统计学上显著增加了2倍,而血糖正常的超重成年人风险增加了50%。血糖升高的体重正常成年人没有额外的癌症风险。BMI和WHtR的影响相互独立。最后,血糖升高的超重女性患女性生殖系统癌症(宫颈癌、子宫内膜癌、子宫癌)和绝经后乳腺癌的风险增加了2.6倍[95%置信区间(CI),1.4 - 4.9],而血糖正常的超重女性风险仅增加了70%(95% CI,1.1 - 2.5)。
这些结果表明,代谢健康的超重/肥胖老年人患癌症的风险可能低于有代谢功能障碍的超重/肥胖成年人。
代谢功能障碍和肥胖协同作用增加癌症风险。