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To examine the combined influence of alcohol use and comorbidity on 20-year mortality in older adults (average age 66 at the time of the baseline survey). DESIGN: Longitudinal analysis of a national probability sample-based cohort study. SETTING: Data sources were the National Health and Nutrition Examination Survey I (NHANES I), 1971-1974, and the NHANES Epidemiologic Followup Survey, 1992. PARTICIPANTS: Four thousand six hundred ninety-one adults aged 60 and older who provided data on alcohol use. MEASUREMENTS: The prevalence of at-risk drinking in older adults in the United States and the 20-year all-cause mortality risk associated with it. At-risk drinking status was determined from amount of alcohol consumed and comorbidities, using a previously validated method. RESULTS: The prevalence of at-risk drinking in the United States between 1971 and 1974 in older adults was 10% (18% of men, 5% of women). The majority of at-risk drinkers were identified as such because of their use of alcohol in amounts deemed risky in the presence of relevant comorbidities (69%) (e.g., drinking 2-3 drinks per day and having gout or anxiety or taking a medication for pain). In men, at-risk drinking was associated with higher mortality rates than not-at-risk drinking (hazard ratio=1.20, 95% confidence interval=1.01-1.41); abstinence was not associated with greater mortality. In women, neither abstinence nor at-risk drinking was associated with greater mortality rates. CONCLUSION: In this first, large population-based study of older adults examining the mortality risks of alcohol use and comorbidity, at-risk drinking was associated with greater mortality rates in men. These findings suggest that a lower threshold of alcohol use should be recommended for older adults with specific comorbidities to reduce mortality risks.

Increases in cytoplasmic Ca2+ concentration ([Ca2+]i) can lead to neuron death. Preventing a rise in [Ca2+]i by removing Ca2+ from the extracellular space or by adding Ca2+ chelators to the cytosol of target cells ameliorates the neurotoxicity associated with [Ca2+]i increases. Another potential route of decreasing the neurotoxic impact of Ca2+ is to overexpress one of the large number of constitutive calcium-binding proteins. Previous studies in this laboratory demonstrated that overexpression of the gene for the calcium-binding protein calbindin D28K, via herpes simplex virus (HSV) amplicon vector, increases the survival of hippocampal neurons in vitro following energetic or excitotoxic insults but not following application of sodium cyanide. We now report that in vivo hippocampal infection with the calbindin D28K HSV vector increases neuronal survival in the dentate gyrus after application of the antimetabolite 3-acetylpyridine and increases transsynaptic neuronal survival in area CA3 following kainic acid neurotoxicity. The protective effects of infection with the calbindin D28K vector in an intact brain may prove to be beneficial during changes in Ca2+ homeostasis caused by neurological trauma associated with aging and certain neurological diseases. [ABSTRACT FROM AUTHOR]