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Delayed Effects of Obese and Overweight Population Conditions on All-Cause Adult Mortality Rate in the USA

机译:肥胖和超重人口状况对美国全因成年死亡率的延迟影响

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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 Behavioral Risk Factor Surveillance System 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.
机译:目前,很少有研究将病理性肥胖和超重体重指数(BMI)与成人全因死亡率联系起来。因此,本文利用美国50个州和哥伦比亚特区的年度行为危险因素监视系统数据,估计了将美国成年人超重(25≤BMI <30)和肥胖率(BMI≥30)与肥胖率联系起来的经验回归模型。全因死亡率。来自未消耗热量的摄入(净能量存储)的多期累积脂肪(饱和脂肪酸)的生物化学为追踪不健康的BMI到全因死亡率提供了自然的理论基础。分别评估肥胖和超重BMI对全因死亡率的延迟影响的横截面和面板数据回归模型。通过控制经济,社会人口统计学和其他因素对全因死亡率的独立影响,我们的发现证实了估计的面板数据模型更为合适。面板数据回归结果表明,肥胖与死亡之间的联系在疾病多年后明显增强。据推测,由于肥胖明显多于人,因此对肥胖的死亡率响应更快。与假定静态(而不是延迟)作用的以往研究相比,该研究中成年人口BMI病理学的统计学显着滞后作用是新颖而有见地的。而且,正如预期的那样,这些滞后效应在肥胖人群中比在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主张及时进行生活方式改变干预措施(例如戒烟)以减慢与不健康BMI相关的过早死亡的临床科学文献相一致。

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