Cognitive assessment appropriate for diagnosis of dementia and CIND in large population surveys could be improved with more targeted information from informants and additional cognitive tests targeting other areas of brain function.

Summary Mice and humans with Growth Hormone Receptor/IGF-1 deficiencies display major reductions in age-related diseases. Because protein restriction reduces GHR-IGF-1 activity, we examined links between protein intake and mortality. Respondents (n=6,381) aged 50–65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer and diabetes mortality during an 18 year follow up period. These associations were either abolished or attenuated if the source of proteins was plant-based. Conversely, in respondents over age 65, high protein intake was associated with reduced cancer and overall mortality. Mouse studies confirmed the effect of high protein intake and the GHR-IGF-1 axis on the incidence and progression of breast and melanoma tumors, and also the detrimental effects of a low protein diet in the very old. These results suggest that low protein intake during middle age followed by moderate protein consumption in old subjects may optimize healthspan and longevity.

Most explanations of the increase in life expectancy at older ages over history emphasize the importance of medical and public health factors of a particular historical period. We propose that the reduction in lifetime exposure to infectious diseases and other sources of inflammation--a cohort mechanism--has also made an important contribution to the historical decline in old-age mortality. Analysis of birth cohorts across the life-span since 1751 in Sweden reveals strong associations between early-age mortality and subsequent mortality in the same cohorts. We propose that a "cohort morbidity phenotype" represents inflammatory processes that persist from early age into adult life.

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Empirical findings do not support recent compression of morbidity when morbidity is defined as major disease and mobility functioning loss.

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There is remarkable consistency in direction of gender differences in health across these 13 countries. The size of the differences is affected in many cases by the similarity in behaviours of men and women.

survive to old age, their mortality rates converge toward those for older whites, although blacks remain disadvantaged (Elo and Preston 1994).The racial gap in mortality during the prime adult ages points to the need to understand chronic health problems of middleaged blacks and whites. Middle age, defined here as ages 51 to 63, designates the lifecycle period when the racial gap in health is potentially at its greatest (House et al. 1994). Our overall goal is to identify racial differences in "life without health problems" to better specify the pathways that lead to racial differences in mortality and to differences in the quality of life lived. We define health problems broadly to include the major fatal and nonfatal chronic diseases, conditions, and impairments, functional difficulty, and disability.Two basic questions guide our analysis. First, are blacks consistently disadvantaged relative to whites across all major chronic eath truncates the lives of black Americans at younger ages than whites, with greater racial differences observed for men than women. National life table estimates for 1996 predict a life expectancy at birth for black men of 66 years compared with almost 74 years for white men (Ventura et al. 1997). Much of this difference is due to the racial disparity in mortality rates prior to age 65. Should blacks D