Dying Slowly But Surely: A Multi-Period Model of the Delayed Effects of Pathological BMI on All-Cause Mortality of US Adults, 2000-2005

Medical and the social science disciplines, together with the global bodies (e.g., The UN Food and Agriculture Organization, and The World Health Organization) focusing on human health conditions, agree that the rising obesity epidemic (the US, worldwide) and related ill-health outcomes (e.g., poor quality of life, atrophied labor productivity, preventable mortality and morbidity) are increasingly problematic. The resource costs of unhealthy Body Mass Index (BMI) for individuals and the society (DHHS, Healthy People 2010. Washington, DC: USGPO, November 2000) are high and rising. The BMI, a measure adjusting body weight (lbs. or kgs.) for height (ft. or m.), classifies individuals as 'not overweight/obese' (BMI= 30). The wider human health and medical literature increasingly links specific-cause and all-cause mortality to unhealthy BMI values. Since the mid 1980s, poor diet and physical inactivity ranked second, next to tobacco, as the second leading actual causes of death in the US (National Center for Chronic Disease Prevention and Health Promotion, 2000). Heart disease, cancer, and stroke, the three leading causes of US deaths, are positively correlated with the conditions of being overweight and obese. Obesity has been linked to almost all causes of death and morbidity, including chronic respiratory diseases and diabetes (respectively, also the 4th and 6th leading cause of deaths in the US in 2000). This paper constructs for econometric estimation a model linking all-cause mortality to the BMI measures of 'overweight' and 'obese'. Data are taken from the Behavioral Risk Factor Surveillance System, for six years 2000 through 2005 across 50 US states and the DC) for which BMI data are consistently reported. The biochemistry of cumulative adiposity (saturated fatty acid) from unexpended caloric intakes (net energy storage) provides the natural theoretical basis for linking pathological BMI to all-cause mortality in US adults. Specifically, biochemistry theory (Speakman, 2005) posits that lifetime expenditure of energy per gram of tissue is not independent of body mass, tissue in smaller animals expends more energy before expiring than tissue in larger animals, and smaller individuals with higher rates of metabolism live longer than their slower counterparts that are larger. (Controls include a set of other independent effects, e.g., education levels, tobacco usage, race/ethnic groups, EPA designated number of toxic waste sites per square mile area, urbanization, others). The regression experiment tested for, confirmed, and adjusted the model for skewed distribution of all-cause mortality per 100,000 population data using the Box-Cox power family of response transformation to symmetry methodology. Relevant econometric model tests confirm cross-sectional models as misspecified. As a result, the Newey-West covariance estimator regression results are reported. Panel data estimates incorporating distributed lag effects of pathological BMI values (obese, overweight) confirm that obesity gradually transits to final mortality significantly over multiple time periods. This is a novel finding in the health economics literature on the obesity mortality link. The paper concludes on the policy responses to the differences in health and economic consequences of unhealthy BMI for the 'overweight' and 'obese' in the US population.