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This paper re-examines health-growth relationship using an unbalanced panel of 17 advanced economies for the period 1870-2013 and employs panel generalised method of moments estimator that takes care of endogeneity issues, which arise due to reverse causality. We utilise macroeconomic data corresponding to inflation, government expenditure, trade and schooling in sample countries that takes care of omitted variable bias in growth regression. With alternate model specifications, we show that population health proxied by life expectancy exert a positive and significant effect on both real income per capita as well as growth. Our results are in conformity with the existing empirical evidence on the relationship between health and economic growth, they, however, are more robust due to the presence of long-term data, appropriate econometric procedure and alternate model specifications. We also show a strong role of endogeneity in driving standard results in growth empirics. In addition to life expectancy, other constituent of human capital, education proxied by schooling is also positively associated with real per capita income. Policy implication that follows from this paper is that per capita income can be boosted through focussed policy attention on population health. The results, however, posit differing policy implications for advanced and developing economies.

Life expectancy at birth in the United States will likely surpass 80 years in the coming decade. Yet recent studies suggest that longevity gains are unevenly shared across age and socioeconomic groups. First, mortality in midlife has risen among non-Hispanic whites. Second, low-educated whites have suffered stalls (men) or declines (women) in adult life expectancy, which is significantly lower than among their college-educated counterparts. Estimating the number of life years lost or gained by age and cause of death, broken down by educational attainment, is crucial in identifying vulnerable populations. Using U.S. vital statistics data from 1990 to 2010, this study decomposes the change in life expectancy at age 25 by age and cause of death across educational attainment groups, broken down by race and gender. The findings reveal that mortality in midlife increased for white women (and to a lesser extent men) with 12 or fewer years of schooling, accounting for most of the stalls or declines in adult life expectancy observed in those groups. Among blacks, mortality declined in nearly all age and educational attainment groups. Although an educational gradient was found across multiple causes of death, between 60 and 80 percent of the gap in adult life expectancy was explained by cardiovascular diseases, smoking-related diseases, and external causes of death. Furthermore, the number of life years lost to smoking-related, external, and other causes of death increased among low- and high school-educated whites, explaining recent stalls or declines in longevity. Large segments of the American population-particularly low- and high school-educated whites under age 55-are diverging from their college-educated counterparts and losing additional years of life to smoking-related diseases and external causes of death. If this trend continues, old-age mortality may also increase for these birth cohorts in the coming decades.

Background We appraised time trends of Japanese life expectancy (LE) and healthy life expectancy (HALE) by gender, LE-HALE and (LE-HALE)/LE figures, along with the women–men’s differences. Methods Using the Japanese LE and HALE values from 1990 through 2013 by gender in the article by the GBD 2013 DALYs and HALE Collaborators, we examined trends of LE and HALE, and their 5- or 3-year changes. We also probed LE-HALE and (LE-HALE)/LE values, and the women–men’s differences. Results LE consistently elongated as reported 76.0, 76.5, 77.6, 78.7, 79.3 and 80.1 years for men from 1990 to 2013; and 82.0, 82.8, 84.3, 85.5, 86.1 and 86.4 years for women, respectively. Both time trends demonstrated a significant linear increase ( p for trend < 0.001). LE changes were 0.4, 1.1, 1.1, 0.7 and 0.7 years for men, and 0.9, 1.5, 1.2, 0.6 and 0.3 years for women. The trends were statistically significant ( p  < 0.001), except for 2010–2013 partly due to 3-year interval. HALE also steadily lengthened as seen 68.1, 68.4, 69.1, 69.9, 70.8 and 71.1 years for men from 1990 through 2013; and 72.2, 72.9, 74.0, 74.8, 75.4 and 75.6 years for women. Both time trends showed almost a linear increase ( p  < 0.05). HALE changes were 0.4, 0.6, 0.8, 0.9 and 0.3 years for men, and 0.7, 1.0, 0.8, 0.6 and 0.2 years for women, without statistical significant trends. LE-HALE values were 8.0, 8.0, 8.5, 8.8, 8.6 and 8.9 years for men; and 9.7, 9.9, 10.4, 10.7, 10.7 and 10.8 years for women. (LE-HALE)/LE figures were 10.5, 10.5, 10.9, 11.1, 10.8 and 11.2% for men, and 11.9, 12.0, 12.3, 12.5, 12.4 and 12.5% for women. LE women–men’s differences were 5.9, 6.4, 6.8, 6.8, 6.8 and 6.3 years, and the HALE figures were 4.2, 4.5, 4.9, 4.9, 4.6 and 4.5 years. Conclusions LE and HALE consistently linearly elongated for both sexes over the study period. Not only LE-HALE but also (LE-HALE)/LE values were still growing for both sexes. Public health measures, nursing-care/services as well as social security schemes are called for to further elevate longevities, HALE in particular, and enhance quality of life and well-being.

A number of indices exist to calculate lifespan variation, each with different underlying properties. Here, we present new formulae for the response of seven of these indices to changes in the underlying mortality schedule (life disparity, Gini coefficient, standard deviation, variance, Theil's index, mean logarithmic deviation, and interquartile range). We derive each of these indices from an absorbing Markov chain formulation of the life table, and use matrix calculus to obtain the sensitivity and the elasticity (i.e., the proportional sensitivity) to changes in age-specific mortality. Using empirical French and Russian male data, we compare the underlying sensitivities to mortality change under different mortality regimes to determine the conditions under which the indices might differ in their conclusions about the magnitude of lifespan variation. Finally, we demonstrate how the sensitivities can be used to decompose temporal changes in the indices into contributions of age-specific mortality changes. The result is an easily computable method for calculating the properties of this important class of longevity indices.

To analyze the gender difference in life expectancy in Chinese urban people and explore the age-specific and cause-specific contributions to the changing gender differences in life expectancy. Data of life expectancy and mortality were obtained from \"Annual statistics of public health in China.\" The gender difference was analyzed by decomposition method, including age-specific decomposition and cause-specific decomposition. Women lived much longer than men in Chinese urban areas, with remarkable gains in life expectancy since 2005, respectively. The gender difference reached a peak in 2007. Mortality difference between men and women in the 60-79 age group made the largest contributions to the gender gap in life expectancy in all 6 years. Among causes of death, cancers, circulatory diseases and respiratory diseases made the largest contributions to the gender gap. 33-38% of the gender gap were caused by cancers, among which lung cancer contributed 0.6 years of the overall gap. The contribution of cancers to the gender gap reduced over time, mostly influenced by the narrowing effect of liver cancer on gender gap. Traffic accidents and suicide were the external causes influencing the gender gap, contributing 10-16% of the overall difference. Public health efforts to reduce excess mortalities for cancers, circulatory disease, respiratory diseases, and suicide among men in particular might further narrow the gender gap in life expectancy in Chinese cities.

In this study, we shed light on the interdependency of child growth, morbidity and life expectancy in the fisher-hunter-gatherers of the Jabuticabeira II shell mound (1214-830 cal B.C.E. - 118-413 cal C.E.) located at the South Coast of Brazil. We test the underlying causes of heterogeneity in frailty and selective mortality in a population that inhabits a plentiful environment in sedentary settlements. We reconstruct osteobiographies of 41 individuals (23 adults and 18 subadults) using 8 variables, including age-at-death, stature, non-specific stress markers (cribra orbitalia, porotic hyperostosis, periosteal reactions, periapical lesions and linear enamel hypoplasia), as well as weaning patterns based on stable isotope data to examine how stress factors module growth and survival. Our results show that shorter adult statures were linked to higher morbidity around weaning age and higher chances of dying earlier (before 35 years) than taller adult statures. In addition, short juvenile stature was related to physiological stressors and mortality. The adult \"survivors\" experienced recurrent periods of morbidity during childhood and adulthood, possibly associated with the high parasite load of the ecosystem and dense settlement rather than to malnourishment. An association between early-stress exposure and premature death was not demonstrated in our sample. To explain our data, we propose a new model called \"intermittent stress of low lethality\". According to this model, individuals are exposed to recurrent stress during the juvenile and adult stages of life, and, nevertheless survive until reproductive age or later with relative success.

Estimate the Years of Life Lost (YLL) for overall and avoidable causes of death (CoD) in Colombia for the period 1998-2011. From the reported deaths to the Colombian mortality database during 1998-2011, we classified deaths from avoidable causes. With the reference life table of the Global Burden of Disease (GBD) 2010 study, we estimated the overall YLL and YLL due to avoidable causes. Calculations were performed with the difference between life expectancy and the age of death. Results are reported by group of cause of death, events, sex, year and department. Comparative analysis between number of deaths and YLL was carried out. A total of 83,856,080 YLL were calculated in Colombia during period 1998-2011, 75.9% of them due to avoidable CoD. The year 2000 reported the highest number of missed YLL by both overall and avoidable CoD. The departments with the highest YLL rates were Caquetá, Guaviare, Arauca, Meta, and Risaralda. In men, intentional injuries and cardiovascular and circulatory diseases had the higher losses, while in women YLL were mainly due to cardiovascular and circulatory diseases. The public health priorities should focus on preventing the loss of YLL due to premature death and differentiated interventions by sex.

It has been noted that national life expectancies have diverged in Europe in recent decades, but it is unknown how these recent trends compare to longer term developments. Data on life expectancy, cause-specific mortality and determinants of mortality were extracted from harmonized international data-bases. Variation was quantified with the inter-quartile range, and the contribution of changing economic conditions was analyzed by comparing observed life expectancy variations with those expected on the basis of changes in levels of national income and/or changes in the relation between national income and life expectancy. During the first decades of the 20 th century, variation in life expectancy in Europe increased to reach peak values around 1920, then decreased to reach its lowest values in 1960 (among men) and 1970 (among women), and finally increased strongly again. The first widening was due to less rapid decline in mortality in Southern and Central and Eastern Europe, particularly from infectious diseases, and coincided with an increasing strength of the national income—life expectancy relation. The second widening was due to stagnating or increasing mortality in Central and Eastern Europe, particularly from cardiovascular diseases, and coincided with a very strong rise of between-country differences in national income. Despite some similarities, differences between both episodes of widening differences in life expectancy cast doubt on the idea that the current episode of widening represents a simple delay of epidemiological transitions. Instead, it is an alarming phenomenon that should be a main focus of European policy making.