Childhood and later life stressors and increased inflammatory gene expression at older ages.

Adverse experiences in early life have the ability to "get under the skin" and affect future health. This study examined the relative influence of adversities during childhood and adulthood in accounting for individual differences in pro-inflammatory gene expression in late life. Using a pilot-sample from the Health and Retirement Study (N = 114) aged from 51 to 95, OLS regression models were run to determine the association between a composite score from three proinflammatory gene expression levels (PTGS2, ILIB, and IL8) and 1) childhood trauma, 2) childhood SES, 3) childhood health, 4) adult traumas, and 5) low SES in adulthood. Our results showed that only childhood trauma was found to be associated with increased inflammatory transcription in late life. Furthermore, examination of interaction effects showed that childhood trauma exacerbated the influence of low SES in adulthood on elevated levels of inflammatory gene expression-signifying that having low SES in adulthood was most damaging for persons who had experienced traumatic events during their childhood. Overall our study suggests that traumas experienced during childhood may alter the stress response, leading to more sensitive reactivity throughout the lifespan. As a result, individuals who experienced greater adversity in early life may be at higher risk of late life health outcomes, particularly if adulthood adversity related to SES persists.

Evidence of accelerated aging among African Americans and its implications for mortality.

Blacks experience morbidity and mortality earlier in the life course compared to whites. Such premature declines in health may be indicative of an acceleration of the aging process. The current study uses data on 7644 black and white participants, ages 30 and above, from the third National Health and Nutrition Examination Survey, to compare the biological ages of blacks and whites as indicated from a combination of ten biomarkers and to determine if such differences in biological age relative to chronological age account for racial disparities in mortality. At a specified chronological age, blacks are approximately 3 years older biologically than whites. Differences in biological age between blacks and whites appear to increase up until ages 60-65 and then decline, presumably due to mortality selection. Finally, differences in biological age were found to completely account for higher levels of all-cause, cardiovascular and cancer mortality among blacks. Overall, these results suggest that being black is associated with significantly higher biological age at a given chronological age and that this is a pathway to early death both overall and from the major age-related diseases.

The role of physiological markers of health in the association between demographic factors and periodontal disease.

BACKGROUND AND OBJECTIVE: Age is highly related to oral health status. The higher prevalence of oral disease within subgroups of the population may reflect a tendency towards "early aging" and dysregulation of multiple physiological systems. This study examines whether the association between periodontal disease and demographic factors is mediated by physiological measures of health. MATERIAL AND METHODS: Logistic regression was used to examine whether biomarkers and demographic factors, such as socio-economic status (SES) and race/ethnicity, were associated with periodontal disease, and then whether the strength of these relationships could be attributed to associations between demographic variables and physiological measures of systemic health. RESULTS: Periodontal disease was associated with measures of SES and race/ethnicity. Furthermore, 1-unit increases in cytomegalovirus (CMV), optical density, C-reactive protein (CRP) and glycated hemoglobin (HbA1c) were associated with a 25% [odds ratio (OR) = 1.25; 95% confidence interval (CI): 1.14-1.36], 13% (OR = 1.13; 95% CI = 1.03-1.24) and 19% (OR = 1.19; 95% CI = 1.12-1.27) increased likelihood of periodontal disease, respectively. However, when biomarkers and socio-demographic variables were both included in the model, their associations with periodontal disease were significantly reduced or eliminated. CONCLUSIONS: The risk of periodontal disease is higher among black and/or low-income individuals; however, these associations appear to be partly due to the greater probability of elevated levels of CRP, CMV or HbA1c among these groups.

Sarcopenic obesity and cognitive functioning: the mediating roles of insulin resistance and inflammation?

This study examined the influence of insulin resistance and inflammation on the association between body composition and cognitive performance in older adults, aged 60-69 and aged 70 and older. Subjects included 1127 adults from NHANES 1999-2002. Body composition was categorized based on measurements of muscle mass and waist circumference as sarcopenic nonobese, nonsarcopenic obese, sarcopenic obese, and normal. Using OLS regression models, our findings suggest body composition is not associated with cognitive functioning in adults ages 60-69; however, for adults aged 70 and over, sarcopenia and obesity, either independently or concurrently, were associated with worse cognitive functioning relative to non-sarcopenic non-obese older adults. Furthermore, insulin resistance accounted for a significant proportion of the relationship between cognitive performance and obesity, with or without sarcopenia. Additionally, although high CRP was significantly associated with poorer cognitive functioning in adults ages 60-69, it did not influence the association between body composition and cognitive performance. This study provides evidence that age-related physiological maladaptations, such as metabolic deregulation, which are associated with abdominal fat, may simultaneously contribute to lower cognition and muscle mass, reflecting a degradation of multiple physiological systems.

Early cohort mortality predicts the rate of aging in the cohort: a historical analysis.

Early environmental influences on later-life health and mortality are well recognized in the doubling of life expectancy since 1800. To further define these relationships, we analyzed the associations between early-life mortality and both the estimated mortality level at age 40 and the exponential acceleration in mortality rates with age characterized by the Gompertz model. Using mortality data from 630 cohorts born throughout the 19th and early 20th century in nine European countries, we developed a multilevel model that accounts for cohort and period effects in later-life mortality. We show that early-life mortality, which is linked to exposure to infection and poor nutrition, predicts both the estimated cohort mortality level at age 40 and the subsequent Gompertz rate of mortality acceleration during aging. After controlling for effects of country and period, the model accounts for the majority of variance in the Gompertz parameters (about 90% of variation in the estimated level of mortality at age 40 and about 78% of variation in the Gompertz slope). The gains in cohort survival to older ages are entirely due to large declines in adult mortality level, because the rates of mortality acceleration at older ages became faster. These findings apply to cohorts born in both the 19th century and the early 20th century. This analysis defines new links in the developmental origins of adult health and disease in which effects of early-life circumstances, such as exposure to infections or poor nutrition, persist into mid-adulthood and remain evident in the cohort mortality rates from ages 40 to 90.

Sex differences in the association between muscle quality, inflammatory markers, and cognitive decline.

OBJECTIVE: Aspects of frailty such as sarcopenia and dementia are associated with a proinflammatory state; however, little research has examined the concurrence of these pathologies. This study examined sex-specific differences in the relationship between low muscle quality and impaired cognitive functioning, while considering the role of inflammatory markers. DESIGN: The nationally representative sample was drawn from a cross-sectional study. PARTICIPANTS: Four hundred forty-five females and four hundred twenty-two males over age 60 from the National Health and Nutrition Examination Survey for 2001-2002 were included. MEASUREMENTS: Muscle quality was calculated as isokinetic strength per unit muscle mass. Skeletal muscle mass of the legs was measured using dual energy x-ray absorptiometry and isokinetic strength of the knee extensors was estimated using a Kin-Com dynamometer. Participants were assessed for cognitive functioning using the Wechsler Adult Intelligence Scale, Third Edition (WAIS-III) Digit Symbol - Coding module. High sensitivity C-reactive protein (CRP) assays were performed on blood samples using a Behring Nephelometer to estimate levels of inflammation. Sex stratified ordinary least squares regression models were utilized to estimate the relationship between muscle quality and cognitive functioning, while examining CRP as a possible mechanism and controlling for potential confounds. RESULTS: In the first model a statistically significant positive relationship was found between cognitive functioning and muscle quality for both sex groups. In the second model, CRP was found to have a statistically significant negative association with cognitive functioning for females but not males. Furthermore, the inclusion of CRP in the second model significantly reduced the predictive power of muscle quality for females, as compared to model 1. CONCLUSION: Measures of sarcopenia are associated with lower cognitive functioning in older adults, and for females, this association may be partly due to systemic inflammation. Further research is need to examine the relationship between these frailty-related pathologies, which have substantial health and economic implications.

Lingering prenatal effects of the 1918 influenza pandemic on cardiovascular disease.

Prenatal exposure to the 1918 influenza pandemic (Influenza A, H1N1 subtype) is associated with ⩾20% excess cardiovascular disease at 60 to 82 years of age, relative to cohorts born without exposure to the influenza epidemic, either prenatally or postnatally (defined by the quarter of birth), in the 1982-1996 National Health Interview Surveys of the USA. Males showed stronger effects of influenza on increased later heart disease than females. Adult height at World War II enlistment was lower for the 1919 birth cohort than for those born in adjacent years, suggesting growth retardation. Calculations on the prevalence of maternal infections indicate that prenatal exposure to even uncomplicated maternal influenza may have lasting consequences later in life. These findings suggest novel roles for maternal infections in the fetal programming of cardiovascular risk factors that are independent of maternal malnutrition.

Summary measures of population health: addressing the first goal of healthy people 2010, improving health expectancy.

This report is one of several Healthy People Statistical Notes that evaluate methodological issues pertaining to summary measures - statistics that combine mortality and morbidity data to represent overall population health in a single number. This report evaluates the consequences of changes in the components of health expectancy measures (i.e., mortality or morbidity) on the overall measure. Any activity limitation is used as a morbidity measure. Simulations are used to evaluate the impacts of reducing 1995 age-specific mortality or activity limitation rates by 5, 10, 25, and 50 percent at all ages. Then it is limited to ages under 25 years, 25 -64 years, and over 64 years. The impact of completely eliminating mortality or activity limitation for the younger age groups is also examined. In general, reducing morbidity rates results in greater changes than the same percent reduction in death rates. The same proportional reduction in age-specific rates for either mortality or morbidity has a greater impact if it occurs at older ages. Reducing mortality results in a greater change in life expectancy than in health expectancy and a decline in the proportion of life lived in healthy states. Reducing morbidity increases both health expectancy and the proportion of life lived in healthy states. Simultaneous reductions in mortality and morbidity have additive effects on health expectancy.

Trends in healthy life expectancy in the United States, 1970-1990: gender, racial, and educational differences.

This paper examines healthy life expectancy by gender and education for whites and African Americans in the United States at three dates: 1970, 1980 and 1990. There are large racial and educational differences in healthy life expectancy at each date and differences by education in healthy life expectancy are even larger than differences in total life expectancy. Large racial differences exist in healthy life expectancy at lower levels of education. Educational differences in healthy life expectancy have been increasing over time because of widening differentials in both mortality and morbidity. In the last decade, a compression of morbidity has begun among those of higher educational status; those of lower status are still experiencing expansion of morbidity.

Does childhood health affect chronic morbidity in later life?

Our analysis examines whether childhood health has long-term and enduring consequences for chronic morbidity. As a part of this analysis, we address two methodological issues of concern in the literature. Is adult height a surrogate for childhood health experiences in modeling chronic disease in later life? And, are the effects of adult socioeconomic status on chronic disease overestimated when childhood health is not accounted for? The analysis is based on a topical module to the third wave of the Health and Retirement Study, a representative survey of Americans aged 55-65 in 1996. Our results support the hypothesis that poor childhood health increases morbidity in later life. This association was found for cancer, lung disease, cardiovascular conditions, and arthritis/rheumatism. The associations were highly persistent in the face of statistical controls for both adult and childhood socioeconomic status. No support was found for using adult height as a proxy for the effects of childhood health experiences. Further, the effects of adult socioeconomic status were not overestimated when childhood health was excluded from the explanatory models. Our results point to the importance of an integrated health care policy based on the premise of maximizing health over the entire life cycle.

Mortality and health in human life spans.

This paper clarifies the relationship between mortality and morbidity in older human populations by addressing two questions. Do mortality and morbidity change over time in the same way? Are the age patterns of mortality and morbidity similar at the oldest ages? We find that the mortality and morbidity do not necessarily change in the same way and that the age patterns of mortality and morbidity are not the same. Factors responsible for this include population heterogeneity and selectivity, the underlying causes of mortality and morbidity, and the mechanisms causing change in mortality and morbidity.

Social environment effects on health and aging: integrating epidemiologic and demographic approaches and perspectives.

This paper provides an overview of epidemiological and demographic research linking social characteristics of both individuals and communities to differences in both morbidity and mortality risks. Evidence is presented linking three broad aspects of the social environment to health--the network of personal social relationships within which most of us live our lives, individual socioeconomic status (SES), and community-level social characteristics. Large and consistent bodies of literature from both epidemiology and demography provide clear evidence for the generally health-promoting effects of personal social relationships and SES. The bulk of the evidence relates to mortality although both fields have begun to examine other health outcomes, including aspects of physical and cognitive functioning as well as disease outcomes. A smaller but growing body of community-level data, reflecting both the socioeconomic/resource characteristics of these broader communities and, more specifically, social features of these environments, also point to health impacts from these more macro level social environment characteristics. Much remains to be elucidated, however, concerning the actual mechanisms through which something as complex and multifaceted as SES "gets under the skin." This necessarily includes consideration of external characteristics of the environments (both physical and sociocultural) where people live and work, and individual characteristics, as well as possible interactions between these in producing the observed SES gradients in health and mortality. These questions concerning links between social environment conditions and health may be a particularly fruitful area of future collaboration, drawing on the shared interest of demographers and epidemiologists in understanding how different social conditions promote variation in distributions of better versus worse health outcomes within a population.

Trends in health and ability to work among the older working-age population.

OBJECTIVES: Because of recent changes in Social Security regulations that will soon begin to raise the age of eligibility for full retirement benefits, it is important to determine whether health and ability to work at older ages have improved in recent years. METHODS: Individual-level data from the National Health Interview Survey from 1982 through 1993 are used in this analysis. Trends in self-reported ability to work, presence of disease, and causes of actual work limitation are examined. RESULTS: Men and women in their 60s, that is those in the older working ages and younger retirement ages, report significant improvement in their ability to work. The change in work ability is large enough so the percentage unable to work at age 67 in 1993 is lower than the percentage unable to work at age 65 in 1982. This improvement appears to have been similar for racial and ethnic groups and across educational subgroups of the population, although African Americans and those with lower educational attainment are less healthy to begin with. The improvement in health is due to the changing educational composition of the population, which is linked to better life-long health, different occupational circumstances, and better health behaviors. In addition, the improvement in work ability is explained by decline in the prevalence of cerebro/cardiovascular diseases and arthritis. DISCUSSION: The level of observed improvement in work ability means that the legislated rise in age of full eligibility for Social Security benefits should be more than compensated for by the improved ability to work.

Do medical conditions affect cognition in older adults?

Analyses of a nationally representative sample who completed a list recall task (weighted n = 6,446) and 2 mental status tasks (weighted n = 6,646) were conducted to determine whether specific medical conditions such as high blood pressure and diabetes as well as general health ratings predict cognitive performance in adults aged 70 to 103. Presence of stroke and poorer health ratings predicted poorer performance on the 3 tasks. Presence of diabetes predicted poorer performance on recall and 1 mental status task. Age interacted with medical conditions including high blood pressure and diabetes in predicting mental status, with condition-related deficits confined to the younger end of the age continuum. Global health ratings interacted with age, with poorer ratings associated with worse mental status in the younger participants. Findings suggest that stroke and diabetes are associated with cognitive deficits. Some deficits are more pronounced in younger old adults with high blood pressure and poorer health ratings.

Cohort differences in disability and disease presence.

Using the National Health Interview Surveys conducted from 1982 through 1993, this article examines cohort patterns in disability and disease presence for adults born between 1915 and 1959, at ages ranging from 30 to 69 years. In general, disability decreases for cohorts born between 1916 and the early 1940s (for men) or the early 1950s (for women), but begins to increase for cohorts born after those dates. Later-born cohorts have significantly lower levels of some diseases, most importantly cardiovascular diseases, arthritis, and emphysema. However, some diseases and conditions are more prevalent in later-born cohorts: asthma, musculoskeletal disorders, and orthopedic impairments. The results presented here indicate that adults born in the late 1940s and 1950s will be in better cardiovascular health but may be in worse musculoskeletal condition when they enter old age compared with current cohorts of older persons.

Further evidence on recent trends in the prevalence and incidence of disability among older Americans from two sources: the LSOA and the NHIS.

The Longitudinal Study on Aging (LSOA) and the National Health Interview Survey (NHIS) are used to examine change in the prevalence of disability from 1982 through 1993 for persons 70 years of age and over. Changes in the likelihood of becoming disabled and the likelihood of recovering from disability also are investigated with the LSOA. There is some evidence for improving disability status among the old. The prevalence of disability is somewhat lower in more recent years in the NHIS; also, the incidence of disability is lower, and the rate of recovery higher during 1988-90 than in the 1984-86 interval. On the other hand, the prevalence of disability increases at some dates after 1984 in the LSOA sample. In both datasets, there is fluctuation rather than a clear trend in the prevalence of disability. Continued steady improvement in rates of onset and recovery and a consistent trend toward improving prevalence is needed before concluding that we are witnessing the beginning of an ongoing trend toward improving health among the older population.

Loss to folow-up in a sample of Americans 70 years of age and older: The LSOA 1984-1990.

Loss to follow-up is a problem in longitudinal samples, and the literature on response rates in panels of older persons suggests that they may be more vulnerable to nonrandom attrition and its consequent biases. The event history approach used in this study to determine the correlates of nonresponse addresses important shortcomings of previous analyses by incorporating time-varying covariates. Nonresponse is not random; persons of older ages, lower education, who live alone, rent (not own), have more functioning impairments, or have another sample person in the household are more likely to become nonrespondents. However, correction accounting for the effect of these correlates of nonresponse, as well as unobserved characteristics potentially affecting nonresponse, suggests that the association between these characteristics and the probability of nonresponse is not large enough to introduce bias. While these results are not portable to other analyses or panels, they do indicate that in this case, significant nonrandom nonresponse does not bias all related analytic results.

Differentials in active life expectancy in the older population of the United States.

This study clarifies the process by which mortality and disability interact to determine differences in active life expectancy by age, sex, race, and education for the U.S. population 70 years of age and over. The analysis is performed using data from the Longitudinal Study of Aging and multistate life tables constructed using the results of hazard models. Women spend more years than men both active and inactive at every age; however, the proportion of life that is expected to be active is smaller for women. These differences are largely due to mortality differences favoring women. Persons with less than a high school education have shorter total and active life expectancies but similar expected lengths of inactive life compared to those with more than a high school education. There are no significant race differences in total life expectancy for race-education groups of the older population; but Blacks have lower expected active life than non-Blacks because of worse functioning.

Echoes of the baby boom and bust: recent and prospective changes in living alone among elderly widows in the United States.

Today the great majority of noninstitutionalized elderly widows live alone, a striking increase from a quarter-century ago. A noticeable difference has occurred, however, in trends by age; the proportion of the young-old widows living alone is starting to decline, while that of the old-old continues to increase. We use a model suggested by earlier studies to explain the emergence of this difference, and assess the prospects of its continuing over the next three decades. We find that the recent differential change in the proportions of younger and older widows living alone is due primarily to a differential change in kin availability that has emerged as the baby boomers' parents have begun to reach retirement age. Over the next decade, the same type of differential change by age in kin availability will continue; living alone is likely to become less common among young-old than among old-old widows, in a reversal of the pattern of the last quarter-century. In the first two decades of the next century, as the baby boom affects kin availability among the old-old, and as the subsequent baby bust affects that among the young-old, the age pattern of living arrangements among elderly widows will reverse once again.