Okunade Albert A, Rubin Rose M, Okunade Adeyinka K
Department of Economics, Fogelman College of Business and Economics, The University of Memphis , Memphis, TN , USA.
Medical Center, The University of Mississippi School of Medicine , Jackson, MS , USA.
Front Public Health. 2016 Sep 28;4:212. doi: 10.3389/fpubh.2016.00212. eCollection 2016.
Currently, there are few studies separating the linkage of pathological obese and overweight body mass indices (BMIs) to the all-cause mortality rate in adults. Consequently, this paper, using annual data of the 50 US states and the District of Columbia, estimates empirical regression models linking the US adult overweight (25 ≤ BMI < 30) and obesity (BMI ≥ 30) rates to the all-cause deaths rate. The biochemistry of multi-period cumulative adiposity (saturated fatty acid) from unexpended caloric intakes (net energy storage) provides the natural theoretical foundation for tracing unhealthy BMI to all-cause mortality. Cross-sectional and panel data regression models are separately estimated for the delayed effects of obese and overweight BMIs on the all-cause mortality rate. Controlling for the independent effects of economic, socio-demographic, and other factors on the all-cause mortality rate, our findings confirm that the estimated panel data models are more appropriate. The panel data regression results reveal that the obesity-mortality link strengthens significantly after multiple years in the condition. The faster mortality response to obesity detected here is conjectured to arise from the significantly more obese. Compared with past studies postulating a static (rather than delayed) effects, the statistically significant lagged effects of adult population BMI pathology in this study are novel and insightful. And, as expected, these lagged effects are more severe in the obese than overweight population segment. Public health policy implications of this social science study findings agree with those of the clinical sciences literature advocating timely lifestyle modification interventions (e.g., smoking cessation) to slow premature mortality linked with unhealthy BMIs.
目前,很少有研究将病理性肥胖和超重体重指数(BMI)与成年人全因死亡率的联系区分开来。因此,本文利用美国50个州和哥伦比亚特区的年度数据,估计了将美国成年人超重(25≤BMI<30)和肥胖(BMI≥30)率与全因死亡率联系起来的实证回归模型。未消耗热量摄入(净能量储存)产生的多期累积肥胖(饱和脂肪酸)的生物化学为将不健康的BMI与全因死亡率联系起来提供了自然的理论基础。分别针对肥胖和超重BMI对全因死亡率的延迟影响估计了横断面和面板数据回归模型。在控制经济、社会人口统计学和其他因素对全因死亡率的独立影响后,我们的研究结果证实估计的面板数据模型更合适。面板数据回归结果显示,肥胖与死亡率的联系在多年患病后显著增强。此处检测到的对肥胖的更快死亡率反应据推测是由于肥胖程度明显更高。与过去假设静态(而非延迟)影响的研究相比,本研究中成年人口BMI病理的统计显著滞后影响是新颖且有洞察力的。而且,正如预期的那样,这些滞后影响在肥胖人群中比超重人群中更为严重。这项社会科学研究结果的公共卫生政策含义与临床科学文献中的观点一致,即提倡及时进行生活方式改变干预(例如戒烟),以减缓与不健康BMI相关的过早死亡率。