Rosengren A, Teo K, Rangarajan S, Kabali C, Khumalo I, Kutty V R, Gupta R, Yusuf R, Iqbal R, Ismail N, Altuntas Y, Kelishadi R, Diaz R, Avezum A, Chifamba J, Zatonska K, Wei L, Liao X, Lopez-Jaramillo P, Yusufali A, Seron P, Lear S A, Yusuf S
Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.
Population Health Research Institute, McMaster University and Hamilton Health Sciences, Hamilton, ON, Canada.
Int J Obes (Lond). 2015 Aug;39(8):1217-23. doi: 10.1038/ijo.2015.48. Epub 2015 Apr 14.
BACKGROUND/OBJECTIVES: Psychosocial stress has been proposed to contribute to obesity, particularly abdominal, or central obesity, through chronic activation of the neuroendocrine systems. However, these putative relationships are complex and dependent on country and cultural context. We investigated the association between psychosocial factors and general and abdominal obesity in the Prospective Urban Rural Epidemiologic study.
SUBJECTS/METHODS: This observational, cross-sectional study enrolled 151 966 individuals aged 35-70 years from 628 urban and rural communities in 17 high-, middle- and low-income countries. Data were collected for 125 290 individuals regarding education, anthropometrics, hypertension/diabetes, tobacco/alcohol use, diet and psychosocial factors (self-perceived stress and depression).
After standardization for age, sex, country income and urban/rural location, the proportion with obesity (body mass index ≥30 kg m(-)(2)) increased from 15.7% in 40 831 individuals with no stress to 20.5% in 7720 individuals with permanent stress, with corresponding proportions for ethnicity- and sex-specific central obesity of 48.6% and 53.5%, respectively (P<0.0001 for both). Associations between stress and hypertension/diabetes tended to be inverse. Estimating the total effect of permanent stress with age, sex, physical activity, education and region as confounders, no relationship between stress and obesity persisted (adjusted prevalence ratio (PR) for obesity 1.04 (95% confidence interval: 0.99-1.10)). There was no relationship between ethnicity- and sex-specific central obesity (adjusted PR 1.00 (0.97-1.02)). Stratification by region yielded inconsistent associations. Depression was weakly but independently linked to obesity (PR 1.08 (1.04-1.12)), and very marginally to abdominal obesity (PR 1.01 (1.00-1.03)).
Although individuals with permanent stress tended to be slightly more obese, there was no overall independent effect and no evidence that abdominal obesity or its consequences (hypertension, diabetes) increased with higher levels of stress or depression. This study does not support a causal link between psychosocial factors and abdominal obesity.
背景/目的:心理社会压力被认为会通过神经内分泌系统的慢性激活导致肥胖,尤其是腹部肥胖或中心性肥胖。然而,这些假定的关系很复杂,并且取决于国家和文化背景。我们在城乡前瞻性流行病学研究中调查了心理社会因素与全身肥胖和腹部肥胖之间的关联。
受试者/方法:这项观察性横断面研究纳入了来自17个高、中、低收入国家628个城乡社区的151966名35至70岁的个体。收集了125290名个体关于教育、人体测量学、高血压/糖尿病、烟草/酒精使用、饮食和心理社会因素(自我感知压力和抑郁)的数据。
在对年龄、性别、国家收入和城乡位置进行标准化后,肥胖(体重指数≥30kg·m⁻²)的比例从40831名无压力个体中的15.7%增加到7720名长期处于压力个体中的20.5%,种族和性别特异性中心性肥胖的相应比例分别为48.6%和53.5%(两者P<0.0001)。压力与高血压/糖尿病之间的关联往往呈负相关。以年龄、性别、体力活动、教育和地区作为混杂因素估计长期压力的总体影响,压力与肥胖之间不存在持续的关系(肥胖的调整患病率比(PR)为1.04(95%置信区间:0.99 - 1.10))。种族和性别特异性中心性肥胖之间不存在关系(调整PR为1.00(0.97 - 1.02))。按地区分层产生了不一致的关联。抑郁与肥胖有微弱但独立的关联(PR为1.08(1.04 - 1.12)),与腹部肥胖的关联非常微弱(PR为1.01(1.00 - 1.03))。
虽然长期处于压力的个体往往稍微更肥胖,但没有总体独立影响,也没有证据表明腹部肥胖或其后果(高血压、糖尿病)会随着压力或抑郁水平的升高而增加。本研究不支持心理社会因素与腹部肥胖之间存在因果关系。