[Investigation of disability prevalence in men and women of advanced age].

Disability prevalence among men and women are investigated using NLTCS surveys conducted in 1982, 1984, 1989, 1994 and 1999 in the US population, on persons older than 65 years, and data from LSADT surveys conducted in 1995, 1997, 1999 and 2001 in the population of the Danish Twins Registry, on persons older than 75 years. In both surveys women are more disabled than men. The probability of becoming disabled and surviving is higher for women than men. The probability of recovering from a disability differs between the sexes statistically insignificant. No time trends are observed in the probabilities of becoming disabled, reversing disability or dying disabled. Calculations show that a decrease in disability prevalence observed in the USA resulted from a decrease in disability prevalence in ages younger than 65 years. Using LSADT data heritability of disability in women older than 75 years is estimated to be 36% (14%; 54%). In men of the same ages the estimate is 11% (0%; 40%) and for both sexes heritability is estimated at 28% (10%; 45%).

The risk of radiation-induced cerebrovascular disease in Chernobyl emergency workers.

The paper deals with estimating radiation risks of non-cancer diseases of the circulatory system among the Chernobyl emergency workers based on data from the Russian National Medical and Dosimetric Registry. The results for the cohort of 61,017 people observed between 1986 and 2000 are discussed. These are essentially updated results for the similar cohort that was studied by authors earlier in 1986-1996. Newly discovered is the statistically significant dose risk of ischemic heart disease [ERR Gy = 0.41, 95% CI = (0.05; 0.78)]. Confirmation is provided for the existence of significant dose risks for essential hypertension [ERR Gy = 0.36, 95% CI = (0.005; 0.71)] and cerebrovascular diseases [ERR Gy = 0.45, 95% CI = (0.11; 0.80)]. In 1996-2000, the assessed ERR Gy for cerebrovascular diseases was 0.22 with 95% CI = (-0.15; 0.58). Special consideration is given to cerebrovascular diseases in the cohort of 29,003 emergency workers who arrived in the Chernobyl zone during the first year after the accident. The statistically significant heterogeneity of the dose risk of cerebrovascular diseases is shown as a function of the duration of stay in the Chernobyl zone: ERR Gy = 0.89 for durations of less than 6 wk, and ERR Gy = 0.39 on average. The at-risk group with respect to cerebrovascular diseases are those who received external radiation doses greater than 150 mGy in less than 6 wk [RR = 1.18, 95% CI = (1.00; 1.40)]. For doses above 150 mGy, the statistically significant risk of cerebrovascular diseases as a function of averaged dose rate (mean daily dose) was observed: ERR per 100 mGy d = 2.17 with 95% CI = (0.64; 3.69). The duration of stay within the Chernobyl zone itself, regardless of the dose factor, had little influence on cerebrovascular disease morbidity: ERR wk = -0.002, with 95% CI = (-0.004; -0.001). The radiation risks in this large-scale cohort study were not adjusted for recognized risk factors such as excessive weight, hypercholesterolemia, smoking, alcohol consumption, and others.

Modeling the effects of biologically incorporated radionuclides and chronic low-dose ionizing radiation exposure on both cancer and chronic non-cancer diseases.

Efforts to model the health effects of low-dose ionizing radiation (IR) have often focused on cancer. Meanwhile, significant evidence links IR and age-associated non-cancer diseases. Modeling of such complex processes, which are not currently well understood, is a challenging problem. In this paper we briefly overview recent successful attempts to model cancer on a population level and propose how those models may be adapted to include the impact of IR and to describe complex non-cancer diseases. We propose three classes of models which we believe are well suited for the analysis of the health effects in human populations exposed to low-dose IR. These models use biostatistical/epidemiological techniques and mathematical formulas describing the biological mechanisms of the impact of IR on human health. They can combine data from multiple sources and from distinct levels of biological/population organization. The proposed models are intrinsically multivariate and non-linear and capture the dynamic aspects of health change.

Population models for the health effects of ionizing radiation.

In this paper we review recently-developed extension frailty, quadratic hazard, stochastic process, microsimulation, and linear latent structure models, which have the potential to describe the health effects of human populations exposed to ionizing radiation. We discuss the most common situations for which such models are appropriate. We also provide examples of how to estimate the parameters of these models from datasets of various designs. Carcinogenesis models are reviewed in context of application to epidemiologic data of population exposed to ionizing radiation. We also discuss the ways of how to generalize stochastic process and correlated frailty models for longitudinal and family analyses in radiation epidemiology.

Demographic analysis and modeling of human populations exposed to ionizing radiation.

The health effects of ionizing radiation on human populations are often analyzed using epidemiological statistical methods. Because of the complexity of the health consequences of ionizing radiation and the prolonged period during which the consequences emerge, we propose to evaluate these health effects using mathematical models that are based on the best theoretical reasoning and prior biological evidence about disease mechanisms. We believe this will improve the ability of the model to identify health effects and reduce erroneous inferences.

Grade-of-membership sibpair linkage analysis maps IDDM11 to chromosome 14q24.3-q31.

We demonstrate the use of Grade-of-membership (GoM) (Manton et al. 1994) for sibpair linkage analysis: GoM was used to map the IDDM11 locus to the region of chromosome 14q24.3 identified by Field et al. (1996). Haplotype groups were constructed from sib pair information on the number of shared alleles. The sample consisted of 578 sibling pairs found in 246 multiplex IDDM families. Both siblings were diabetic in 53% of the pairs (AA). Pair members could share 0, 1 or 2 alleles IBS at each of eight linked marker loci spanning IDDM11. Three model-based groups best represented the data on allele sharing: the groups corresponded to 'No', 'One' and 'Two' shared haplotypes for the region. Group 'Two' was larger (37% vs. 25%, p < 0.0001) and more homogeneous (p < 0.0001) than expected by chance consistent with the IDDM11 locus being a determinant of diabetes in multiplex families. Genetic linkage of IDDM to the region was demonstrated by a 19% increase in the proportion of AA pairs over the haplotype groups: 'No', 42%; 'One', 49%; 'Two', 61%, p = 0.0005, representing a 43% relative increase.

Changes in the prevalence of chronic disability in the United States black and nonblack population above age 65 from 1982 to 1999.

Survey evidence through the early 1990s generally suggests a reduction in disability in the elderly population of the United States. Because the evidence is not fully consistent, several authors have speculated about whether disability declines will continue. This paper reports results from the 1999 National Long-Term Care Survey on disability trends from 1982 through 1999. It is found that disability continued to decline in the 1994 to 1999 period, and that the decline was greater in the 1990s than in the 1980s. The disability decline from 1982 to 1989 was 0.26% per year, from 1989 to 1994 it was 0.38% per year, and from 1994 to 1999 it was 0.56% per year. In addition, disability declined by a greater percentage for blacks than for nonblacks over the 1989 to 1999 period.

Active life expectancy estimates for the U.S. elderly population: a multidimensional continuous-mixture model of functional change applied to completed cohorts, 1982-1996.

An increment-decrement stochastic-process life table model that continuously mixes measures of functional change is developed to represent age transitions among highly refined disability states interacting simultaneously with mortality. The model is applied to data from the National Long Term Care Surveys of elderly persons in the years 1982 to 1996 to produce active life expectancy estimates based on completed-cohort life tables. At ages 65 and 85, comparisons with extant period estimates for 1990 show that our active life expectancy estimates are larger for both males and females than are extant period estimates based on coarse disability states.

Vitality index in survival modeling: how physiological aging influences mortality.

We investigated the relation of the age trajectory of physiological indicators of the average metabolic activity of organisms in a population to the age-specific population mortality rate. We show that a metabolic rate indicator (MRI) can be estimated using traditional physiological measures, such as homeostatic serum glucose concentration, vital capacity, and such. Estimates of the MRI were made from data collected in the Multiple Risk Factor Intervention Trial (MRFIT) study. The relation of the empirical mortality rate and MRI was also tested using MRFIT data. The age trajectory of MRI was evaluated using Swedish mortality data. The mortality results reproduce the "Strehler and Mildvan effect." The average rate of decline of MRI with age coincides with estimates predicted by Strehler using other methods. Possible extensions of the method are discussed.

Gender differences in the cross-sectional and cohort age dependence of cause-specific mortality: the United States, 1962 to 1995.

OBJECTIVE: Gender- and age-specific mortality rates were calculated to determine the role of behavioral and biologically based differences in health. DESIGN: Changes in age-specific mortality rates were calculated for males and females across select time periods, in addition to gender- and cause-specific mortality age trajectories for birth cohorts for heart disease, stroke, and lung and breast cancer. Differences between cohort mortality age trajectories and the age pattern of mortality rates were related to socioeconomic differences between genders and to biological risk factors. SUBJECTS: U.S. males and females aged 30 to 95+ over the 34-year period 1962 to 1995. METHODS: Gender- and age-specific mortality rates were computed and displayed using the logarithmic transform of the rates for five-year age categories. RESULTS: Major gender cross-sectional mortality differences were found for heart disease, stroke, and lung cancer, with males being disadvantaged except for stroke. Less variation was found for lung cancer in recent male cohorts compared to large rates of change for recent female cohorts. Female breast cancer mortality showed modest variation, with most of the cohort differential in risk in postmenopausal breast cancer risk. Relative risk of lung cancer with age was greater for females. CONCLUSION: Differences in male and female cohort mortality rates underlie many of the period changes for heart disease, stroke, and lung cancer. Cohort differences were largest for lung cancer, although the cohort-specific smoking patterns these rates imply could also be responsible for some of the heart disease and mortality differences. The breast cancer mortality rates showed consistency with the concept of two distinct etiologies for breast cancer: premenopausal and postmenopausal. Large cohort increases in female lung cancer mortality may be alterable by behavioral measures and education.

Changes in home care use by disabled elderly persons: 1982-1994.

OBJECTIVES: The use of, and changes in the use of. formal (paid) and informal care by elderly persons who are chronically disabled and living in the community was studied. METHODS: Estimates were made of the sources and volume of home care use for persons reporting chronic disability in the 1982, 1989, and 1994 National Long Term Care Surveys. Comparisons were made across disability intensity, survey data, and age. RESULTS: The analyses showed changes over time in the sources of home care services. Generally, the combined use of both paid and informal home health care increased, whereas the use of either source of care alone decreased. The amount spent on formal care increased with disability level and age. DISCUSSION: Use of formal sources of care by community disabled elderly residents increased, likely because of changes in the Medicare home health care benefits in 1989. Increased use of home health care was associated with the concurrent use of informal care.

Models for forecasting chronic disease processes in adult and elderly populations: effects of stochasticity.

BACKGROUND: Forecasting the population health burden of chronic diseases requires models consistent with the relation, over time and in an uncertain environment, of risk factors and diseases at the individual level. There is now sufficient longitudinal data, and scientific understanding, of some chronic diseases to construct detailed process-models to better predict their population health burden and more realistically describe the effects of interventions. A crucial clement in constructing models is the way in which stochastic influences are described, e.g. are they allowed to interact over time with deterministic model features? METHODS: A review of statistical and forecasting models aimed to establish what ancillary data and scientific insights are necessary to describe multivariate stochastic health processes and their response to interventions. For circulatory diseases and cancer there exists sufficient longitudinal data and biological insight to construct stochastic multivariate process models. For other diseases, biological knowledge is less complete and there are fewer data sets where multiple risk factors are assessed longitudinally. Forecasting models for those diseases will then rely more heavily on theoretical assumptions about disease behaviour.

Dynamic paradigms for human mortality and aging.

Hazard models are often applied to mortality data of humans and other species so that the parameter estimates made for those models can be used to make inferences about the biology, and comparative biology, of aging processes. Enough longitudinal data on physiological and functional changes in humans now exist to know that the age trajectory of the physiological state of individuals is multidimensional, stochastic, and plastic. Thus, to fully assess the biological significance of existing longitudinal data on human aging and mortality processes, multivariate stochastic process models must be developed that are biologically detailed and valid. This requires assessing genetic mechanisms controlling human longevity and rates of aging, developing models of how those traits may have evolved, and developing statistical methods for identifying gene environment interactions. This article examines the theoretical basis for such models and the biological rationale of their parametric structure. Several examples are given.

The effects of health changes on projections of health service needs for the elderly population of the United States.

The 1982-1994 National Long-Term Care Surveys indicate an accelerating decline in disability among the U.S. elderly population, suggesting that a 1.5% annual decline in chronic disability for elderly persons is achievable. Furthermore, many risk factors for chronic diseases show improvements, many linked to education, from 1910 to the present. Projections indicate the proportion of persons aged 85-89 with less than 8 years of education will decline from 65% in 1980 to 15% in 2015. Health and socioeconomic status trends are not directly represented in Medicare Trust Fund and Social Security Administration beneficiary projections. Thus, they may have different economic implications from projections directly accounting for health trends. A 1.5% annual disability decline keeps the support ratio (ratio of economically active persons aged 20-64 to the number of chronically disabled persons aged 65+) above its 1994 value, 22:1, when the Hospital Insurance Trust Fund was in fiscal balance, to 2070. With no changes in disability, projections indicate a support ratio in 2070 of 8:1-63% below a cash flow balance.

Biodemographic trajectories of longevity.

Old-age survival has increased substantially since 1950. Death rates decelerate with age for insects, worms, and yeast, as well as humans. This evidence of extended postreproductive survival is puzzling. Three biodemographic insights--concerning the correlation of death rates across age, individual differences in survival chances, and induced alterations in age patterns of fertility and mortality--offer clues and suggest research on the failure of complicated systems, on new demographic equations for evolutionary theory, and on fertility-longevity interactions. Nongenetic changes account for increases in human life-spans to date. Explication of these causes and the genetic license for extended survival, as well as discovery of genes and other survival attributes affecting longevity, will lead to even longer lives.

The dynamics of dimensions of age-related disability 1982 to 1994 in the U.S. elderly population.

Declines in chronic disability were observed in the National Long Term Care Survey (NLTCS) 1982 to 1994. We analyzed the 1982, 1984, 1989, and 1994 NLTCS to identify the dimensions of chronic disability from multivariate analyses of a rich battery of measures of the ability (or inability) to perform specific activities. Changes over time in the prevalence of individual disability dimensions can be tracked to evaluate the rate of age-related losses of specific functions, 1982-1994. Seven dimensions described changes in the age dependence of 27 activities of daily living, instrumental activities of daily living, and physical performance measures in community and institutional resident elderly individuals over the 12 year period. Adjusted for age, the healthiest dimension with the best physical function experienced the largest increase in prevalence (3.3%) implying a decline in age-related disability. Disability declines were correlated with reductions in select health conditions (e.g., dementia and circulatory disease) over the study period.

Education-specific estimates of life expectancy and age-specific disability in the U.S. elderly population: 1982 to 1991.

The authors used mortality data for 1982 to 1991 linked to survey records from the 1982, 1984, and 1989 National Long Term Care Surveys to calculate gender differences over age in mortality and functional status for high (8 or more years of schooling) and low (less than 8 years of schooling) education subgroups. Males and females with high education maintained better functioning at later ages than those with low education. The authors also found that mortality was higher, after conditioning on disability, in both the male and female low-education than the male and female high-education groups. The size of the education effect on both disability and mortality was large, for example, about 7.6 years difference in female life expectancy at age 65; a roughly 2-year difference for males.