3
Health and Disability Differences Among Racial and Ethnic Groups

Kenneth G. Manton and Eric Stallard

Introduction

Racial and ethnic differences in the age patterns of incidence and prevalence of chronic morbidity and disability are important because they provide data on (1) biological mechanisms, endogenous and exogenous, of age-related morbidity, (2) how the quality of life for groups changes over age and time, and (3) lead indicators of future mortality and disability trends that aid in the development of health policy by improving mortality, health service, and population forecasts.

We have previously examined epidemiological, demographic, and other data on racial and ethnic health differences (Manton et al., 1987). Here we examine more recent biomedical and epidemiological research on African-American, white, and Hispanic differences in health and disability. Though data on racial and ethnic health differences have improved and have generated many new hypotheses, there are many areas in which no definitive studies have been done for different racial and ethnic groups. Consequently, there is often little consensus on the magnitude or age dependence of racial and ethnic differences in health or on the biological mechanisms underlying many differences.

Since the scientific record on racial and ethnic health differences, especially at late ages, is incomplete, we must assemble available data into a coherent description to compare age-related health differences across racial and ethnic groups. For this purpose, a life-table model of the age relation of three health processes—disability, morbidity, and mortality—is useful. Figure 3-1 portrays changes in two hypothetical cohorts, one with high mortality and one with low mortality, as linked life-table functions.



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--> 3 Health and Disability Differences Among Racial and Ethnic Groups Kenneth G. Manton and Eric Stallard Introduction Racial and ethnic differences in the age patterns of incidence and prevalence of chronic morbidity and disability are important because they provide data on (1) biological mechanisms, endogenous and exogenous, of age-related morbidity, (2) how the quality of life for groups changes over age and time, and (3) lead indicators of future mortality and disability trends that aid in the development of health policy by improving mortality, health service, and population forecasts. We have previously examined epidemiological, demographic, and other data on racial and ethnic health differences (Manton et al., 1987). Here we examine more recent biomedical and epidemiological research on African-American, white, and Hispanic differences in health and disability. Though data on racial and ethnic health differences have improved and have generated many new hypotheses, there are many areas in which no definitive studies have been done for different racial and ethnic groups. Consequently, there is often little consensus on the magnitude or age dependence of racial and ethnic differences in health or on the biological mechanisms underlying many differences. Since the scientific record on racial and ethnic health differences, especially at late ages, is incomplete, we must assemble available data into a coherent description to compare age-related health differences across racial and ethnic groups. For this purpose, a life-table model of the age relation of three health processes—disability, morbidity, and mortality—is useful. Figure 3-1 portrays changes in two hypothetical cohorts, one with high mortality and one with low mortality, as linked life-table functions.

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--> FIGURE 3-1 Interrelations of morbidity, disability, and mortality in two hypothetical populations. SOURCE: Duke University Center for Demographic Studies.

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--> The area between curves for each cohort represents the person-years lived free of morbidity and disability, with morbidity but free of disability, or with both morbidity and disability. The high-mortality cohort reflects a population with more time spent in morbid states but less time spent with disability (e.g., in developing countries, where acute and long-term medical care for disabled elderly persons is scarce, or in socioeconomically disadvantaged groups). The low-mortality cohort spends less time in morbid states, but more time with disability. The first scenario suggests that in populations with low life expectancy, people spend time in clinically latent morbid states and that once disability occurs, the lack of social and long-term care infrastructure causes rapid terminal declines due to a loss of physical homeostasis (e.g., Colantonio et al., 1992). It is uncertain whether this scenario holds for U.S. African Americans and Hispanics who, often socioeconomically disadvantaged over much of the life course, may have greater social resources and relatively equitable access to medical and postacute services at age 65 through Medicare—and to long-term care services through Medicaid. In populations with high life expectancy, health care may defer chronic morbidity to later ages, with disabled people able to live a long time with adequate long-term care. This scenario, however, may not occur even in economically advanced countries. In Japan, one of the world's richest economies, only 6 percent of gross national product was spent on health services in 1990 even though, because of high life expectancy and declining fertility, the population is aging. Consequently, the health services provided to the elderly are limited, with many elderly enduring stays of 6 months or more in acute care hospitals because of a lack of long-term care and rehabilitation facilities (Okamoto, 1992). The two hypothetical models represent scenarios against which the health experience of U.S. racial and ethnic groups can be compared. Race-related physiological differences (e.g., hypertension; Cooper and Rotimi, 1994) may produce more complex scenarios than the ones shown in Figure 3-1, as may differences in access to health care. Ideally, longitudinal data on levels and types of disability, on flows into and out of morbidity and disability states, and on ageand gender-specific effects of diseases on mortality are used to construct such models. For example, a disabling event prevalent in U.S. postmenopausal women is hip fracture. The natural history of hip fractures, like that of other events and conditions, has evolved. The mean age for hip fractures in Britain increased from 67 years in 1944 to 79 years in 1990 (Keene, 1993). This 12-year shift marked a change in hip fracture's natural history. At age 67, hip fractures often do not involve the hip socket and are due to exogenous forces. Hip fractures at later ages often involve the hip socket, are due to osteoporosis, and require more health care. Such age changes in disease presentation could affect U.S. racial and ethnic differences in disability and mortality because African-American and Hispanic females have lower risks of hip fracture than white females.

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--> Unfortunately, longitudinal data are not equally available for the groups reviewed. Consequently, we need to assess the quality and scope of the literature on racial and ethnic differences on specific diseases and conditions and then integrate these various findings. This is a multistep process. First, we review data on the racial and ethnic differences in the risks of specific diseases and in the rates at which the diseases progress. When possible, we make gender-specific comparisons because racial and ethnic health differences often vary in degree, and sometimes in direction, by gender. Since many studies of racial and ethnic groups were done for individual diseases, studies of racial and ethnic differences have to be reviewed for a number of areas. Thus, the first stage of the review provides insight into racial and ethnic differences in disease-specific mechanisms and their age and gender dependence. Since most disease-specific studies are of select populations, as a second stage we review the age relation of racial and ethnic differences in health, disability, and mortality in two sets of national data. First, we examine age patterns of total and cause-specific mortality by race to determine if they are consistent with the epidemiological data on racial and ethnic differences in the age dependence of disease processes. This is logical since racial and ethnic differences in disease in large part cause racial and ethnic differences in mortality age patterns. Second, we examine the National Long Term Care Surveys, where race-specific disability and mortality trajectories can be linked. Thus, an assemblage of data is used to identify (1) the age dependence of disease mechanisms, (2) mortality and morbidity linkages, and (3) disability and mortality linkages. These relations, from different data sets, provide information to construct models like Figure 3-1. Major Morbidity Processes And Their Age Dependence Across Racial And Ethnic Groups There are few studies that describe a number of diseases in a longitudinally followed elderly population. One such study (Guccione et al., 1994), though representing only whites, provides a context in which to discuss racial and ethnic differences in disease. In the study, 2,731 people were followed for 38 years to determine which of 10 conditions caused one or more of seven disabilities in people aged 64 to 98. The proportion of disability due to each condition, adjusted for age, sex, and comorbidity, is presented in Table 3-1. Stroke and heart disease caused disability on all seven functions. Diabetes, osteoarthritis, and hip fracture were also responsible for significant disability. These results suggest that as a minimum, we should examine studies on hip fractures (osteoporosis), stroke, and heart disease in African Americans and Hispanics, and that it would be good to examine atherosclerosis, hypertension, diabetes, and anemia as well. In the review we look for differences between racial and ethnic groups (e.g., hip fractures are more prevalent among white females).

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--> TABLE 3-1 Percentage of Disability Attributable to Specific Conditions After Adjustment for Age, Sex, and Comorbidity, by Condition and Activity for 2,731 Whites Followed for 38 Years in the Framingham Heart Study Activity Knee Osteoarthritis Hip Fracture Diabetes Stroke Heart Disease Congestive Heart Failure Claudication Chronic Obstructive Pulmonary Disease Depressive Symptomatology Cognitive Impairment Stair climbing 16.7 9.1 9.8 12.8 5.2 7.6 3.1 7.4 15.4 —a Walking a mile 15.4 4.9 4.3 9.3 9.3 2.4 6.8 5.2 10.4 —a Heavy home chores —a 2.8 2.2 6.7 15.3 3.9 1.2 3.8 4.0 —a Housekeeping 16.7 7.8 2.6 12.6 13.4 6.5 0.0 6.5 15.9 3.4 Cooking 0.5 7.1 6.8 14.7 8.9 3.3 3.1 —a 4.3 7.3 Grocery shopping 1.2 7.5 3.5 16.7 13.0 1.6 —a 4.5 15.4 7.8 Carrying bundles 16.6 7.3 4.6 12.6 2.3 6.6 3.0 4.0 16.6 8.6 a Adjusted odds ratio < 1; attributable fraction not computable. SOURCE: Guccione et al., 1994:Table 5. Copyright 1994 by the American Public Health Assocation. Reprinted by permission.

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--> We examine age differences in disease as well as risk factors and disease mechanisms. We examine other prevalent diseases (notably cancer) that are not listed in Table 3-1. Also, to describe possible physiological mechanisms, we occasionally refer to cross-national data to distinguish social from physiological factors in racial and ethnic differences in disease. A complication in reviewing disease mechanisms is that there are racial and ethnic differences in disease interactions (e.g., atherosclerosis and osteoporosis, diabetes and stroke), especially at later ages. Osteoporosis and Hip Fracture Osteoporosis is usually viewed as a disease of postmenopausal women that accelerates with age. Two separate mechanisms have been proposed for osteoporosis. One, prevalent from age 55 to 74, is related to bone density and the rapidity of postmenopausal declines in estrogens. A second, dominating after age 75, is due to age differences in vitamin D metabolism (e.g., in the kidney and liver) and intestinal absorption of calcium (Eastell et al., 1991). The morbidity of both types of osteoporosis is manifest in two ways. The first is increased risk of hip, spinal, and wrist fractures. Hip fracture is often studied because its consequences are severe—hip fracture mortality is estimated to be between 5 percent and 20 percent with long-term nursing home care necessary for 15 percent to 33 percent of patients (Boult et al., 1991). Spinal fractures have a slower course. A second effect of osteoporosis is its interaction with atherosclerosis. Here we discuss racial and ethnic differences in the effect of osteoporosis on hip fracture. Interaction with atherosclerosis is deferred to the discussion of heart disease and stroke. Early onset osteoporosis is a disease of postmenopausal women that accelerates with age and is often associated with hip fracture. Hip fracture is more prevalent in white than in African-American or Hispanic women. Hip fracture rates begin to increase exponentially at age 70 for white women. They start to increase exponentially for white men and black women at age 75 and for black men past age 85. Since the incidence rates of hip fracture double every 5 years, this means that white men and black women have half the incidence of white women. Hispanic female rates are similar to black female rates (Kellie and Brody, 1990; Riggs and Melton, 1992). Possible explanations for racial differences in the incidence of hip fracture (and the rate of osteoporotic changes) are differences in bone density at menopause (possibly due to early differences in nutrition, physical activity, and body mass) and in the postmenopausal production of sex and parathyroid hormones. One way to understand physiological differences in osteoporosis in racial and ethnic groups is to examine differences between males and females. The risk of hip fracture is lower, and occurs at later ages, in males than in females. Edelstein and Barrett-Connor (1993) found that body mass relative to height was associated with

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--> bone mineral density for both genders. However, whereas lean body mass predicted bone density in both genders, fat mass predicted a larger proportion of bone mineral density in women than men, possibly because of the conversion of androgens to estrogens in adipose tissue. Thus, both mechanical (i.e., weight-bearing physical activity) and hormonal factors likely affect bone density. To analyze the effect of hormones on bone mineral density in elderly African-American, Hispanic, and white females, researchers often study serum estrone, the dominant type of estrogen produced postmenopausally. In postmenopausal women it is produced by aromatization of androstenedione in adipose (fat) tissue. Cauley et al. (1994) examined serum estrone levels to see if they explained differences in bone mass in black and white females. Serum estrone levels were higher in African-American than in white women, and bone mass was 23 percent to 27 percent greater in black women. Levels of serum estrone were related to bone mass differences among white, postmenopausal women. Bone mass decreased linearly with age for white, but not black, females. This could be due to several factors. Black-white differences in body mass explained most differences in serum estrone. However, nonobese black females had greater bone mass than nonobese white females. Race still significantly predicted bone mass differences after serum estrone was controlled for. Edelstein and Barrett-Connor's (1993) study of gender differences in bone density suggests that female racial differences in bone mass that are not explained by serum estrone might be due to the greater lean body mass of African-American females in comparison with white females and to the mechanical effects of greater muscle mass on physical activity and bone metabolism. The greater bone density of African-American females may be due to higher body mass and to greater postmenopausal production of estrone due to a higher proportion of body fat, factors that could increase the risk of hypertension and adult onset diabetes. If, instead, greater bone density is due to greater lean body mass and physical activity in African-American females, then the metabolic and circulatory effects of a higher body mass would be less likely to cause stroke and heart disease. Other risk factors for African-American women, including thinness, prior stroke, using walking aids, and alcohol consumption, were also risk factors for white women. Lower hip fracture risks for Hispanic females are also associated with greater body mass. Racial and ethnic differences in the risk of osteoporosis and hip fracture among females may involve several additional factors. First, late onset osteoporosis (age 75 and older) is linked to age changes in vitamin D metabolism (in the kidney and liver) and intestinal absorption of calcium (Eastell et al., 1991). Vitamin D increases osteoclastic activity (i.e., a breaking down of the bone matrix by cells in the constant remodeling of bone tissue) and bone resorption (decreases in bone mass). Thus, both too little and too much vitamin D causes osteoporosis (Moon et al., 1992). This effect, however, differs by race. Blacks are less sensitive than whites to both vitamin D toxicity and deficiency (Taussig, 1966; Seelig, 1969). Studies of blacks aged 68

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--> to 93 and whites 70 to 89 showed that hypovitaminosis D with secondary hyperparathyroidism occurred often in blacks (Perry et al., 1993). However, even with lower vitamin D levels, there was less bone resorption (and less turnover of skeletal mass) in U.S. blacks. In native Africans the incidence of hip fracture is even lower—only half that of U.S. blacks. A lower rate of bone formation was also indicated by lower serum osteocalcin in U.S. blacks. Blacks had higher ionized calcium levels than whites with similar parathyroid hormone levels; this suggests that bone metabolism is less sensitive to parathyroid hormone in blacks. The reduced sensitivity may be an adaptation in blacks to (1) a higher melanin content of the skin, which therefore produces less vitamin D, and (2) a lower intake of dairy products because of a high prevalence of intestinal lactase deficiency (Pollitzer and Anderson, 1989). A decreased sensitivity to parathyroid hormone and greater stability of skeletal mass in African-American females thus appear as important in their lower risk of osteoporosis as body mass differences and their effects on the postmenopausal production of sex hormones. Consistent with findings on the two types of osteoporosis, vitamin D and calcium supplementation, at least in white women, decreased hip fracture to advanced ages (e.g., in a group with a mean age of 84; Chapuy et al., 1994). Supplemental estrogens reduced the risk of fracture in black women, as it did for white women, up to age 75 (Grisso et al., 1994). Heart Diseases and Stroke U.S. heart disease and stroke mortality has changed markedly (DeStefano et al., 1993; Ghali et al., 1990; Pathological Determinants of Atherosclerosis in Youth Research Group, 1993). Although U.S. mortality for most types of heart disease and stroke has declined, racial differences in mortality are still marked: the age-adjusted mortality rates from major cardiovascular diseases for blacks is 1.5 times the rate for whites (Singh et al., 1996:Table 12). Congestive heart failure is an exception to the general trend toward lower mortality from cardiovascular disease. Congestive heart failure occurs at late ages and reflects the cumulative effect of prior is chemic heart disease, hypertension, and atherosclerosis. Mortality from congestive heart failure increased until at least 1988 (Centers for Disease Control and Prevention, 1994). Mortality increases were paralleled by increased morbidity and service use and affected all race and gender groups. Age-standardized congestive heart failure hospitalization rates increased 60 percent for both whites and blacks from 1973 to 1986 (Ghali et al., 1990). This is consistent with declines from 1980 to 1989 in nonfatal coronary heart disease at ages 45 to 54—with increases at ages 75 to 84 (DeStefano et al., 1993). Changes in other circulatory diseases differ by race and gender. To better differentiate African-American, Hispanic, and white trends in circulatory disease (Sempos et al., 1988), we identified factors affecting race and age trends of

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--> several processes related to circulatory events: atherosclerosis, diabetes, body iron stores, and hypertension. Atherosclerosis Atherosclerosis is a degenerative process that increases the risk of many circulatory diseases. It affects coronary heart disease, stroke, and, at late ages, peripheral vascular disease. Thus, in some senses the relation of atherosclerosis (the age-dependent process) to heart disease and stroke (the morbid events) parallels the relation of osteoporosis (the age-dependent process) to hip and other fractures (the morbid events). An evaluation of African-American and Hispanic differences in the progression of atherosclerosis is handicapped by a lack of longitudinal studies; the Framingham Heart Study, for example, studied only whites. The two best known longitudinal studies of circulatory disease containing significant numbers of African Americans and whites are the Charleston Heart Study and the Evans County study. There are, however, cross-sectional studies of risk factors for circulatory disease that represent African Americans and whites; a few represent Hispanics. Other studies examine differences in pathologies of the circulatory system in African Americans and whites at death. One widely studied risk factor for atherosclerosis is cholesterol. Some data suggest that atherosclerosis in whites is more susceptible to cholesterol than in blacks (Eggen et al., 1965; Strong, 1972). In the 28-year follow-up of the Charleston Heart Study, the dependence of coronary heart disease mortality on cholesterol differed in African Americans and whites. White female cholesterol values had a J-shaped relation to mortality (i.e., mortality was higher at both very low and very high values of cholesterol). At intermediate values, mortality risk was lowest. The cholesterol-mortality relation was linear for African-American females. The increase in the risk of coronary heart disease with an increase of 1 standard deviation in cholesterol was 60 percent for white, compared with 40 percent for black, females (Knapp et al., 1992). For males, both the Charleston Heart Study and the Evans County Study suggest higher risk of coronary heart disease for whites than for blacks. In Charleston, black men and women had lower total cholesterol at baseline. Cholesterol was not a significant predictor of risk for black males (Keil et al., 1993). To examine African-American, Hispanic, and white differences in the national distribution of, and changes in, total cholesterol, the National Health and Nutrition Examination Surveys for 1976 to 1980 (NHANES II) and for 1988 to 1991 (NHANES III; Sempos et al., 1993) can be used. Declines in cholesterol were similar for whites, African Americans, and Hispanics—though the proportion in a high-risk group was 8 percentage points lower for both African American and Hispanics than for whites. Lower cholesterol levels in African Americans and Hispanics may be due to differences in activity and nutrition. Studies showed that black Seventh Day Adventists with vegetarian (or partly vegetarian)

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--> diets had lower cholesterol than blacks eating an omnivorous diet; that is, a dose-response effect between cholesterol and nutritional factors (e.g., fats) was evident for African Americans as it is for whites (Melby et al., 1994). Total cholesterol is a general indicator of the risk of coronary heart disease. There is growing interest in cholesterol subtypes and other lipoproteins. High-density lipoprotein (HDL) cholesterol protects against atherosclerosis by transporting lipids away from atheromas (irregularly distributed lipid deposits in the large- and medium-sized arteries). Low-density lipoprotein (LDL) cholesterol accelerates atherosclerosis, as may very low density lipoproteins (VLDL) or triglycerides, because LDL is trapped in atheromas after being oxidized. Other lipoproteins—for example, lipoprotein (a) [Lp(a)] or apolipoprotein E (Apo E)—also predict racial differences in atherosclerosis. Lp(a) is associated with heart disease, stroke, and peripheral vascular disease. It appears to prevent blood clots from being dissolved by blocking plasminogen—an enzyme responsible for thrombolysis. It may also increase the uptake of LDLs by atheromas (Valentine et al., 1994). The Atherosclerosis Risk in Communities (ARIC) study (1986 to 1989) of 14,254 persons measured HDL, LDL, and Lp(a) for blacks and whites of both genders. Lp(a) strongly discriminated black and white risks of coronary heart disease. Lp(a) levels were twice as high among blacks of both genders as among whites. Few environmental factors affected Lp(a). Selby et al. (1994) showed that Lp(a) levels had genetic determinants and that levels were higher in African-American than in white women. A genetic determination of Lp(a) levels for U.S. blacks is consistent with findings that blacks from the Sudan (Sandholzer et al., 1991), Ghana (Helmhold et al., 1991), and the People's Republic of the Congo (Parra et al., 1987) had Lp(a) levels similar to U.S. blacks. Also consistent with a genetic determination is the fact that racial differences in Lp(a) levels exist at early ages. The Coronary Artery Risk Development in Young Adults (CARDIA) study of 5,115 persons aged 18 to 30 found mean Lp(a) values twice as high for blacks as for whites—with black medians three times as high—results consistent with the Houston, Texas (Gayton et al., 1985), Bogalusa Heart (Srinivasan et al., 1991), and ARIC studies. HDL and LDL in ARIC, in contrast, were similar for women of both races. Black men had more HDL than white men. White men had 16 percent to 26 percent higher triglyceride levels and the lowest HDL levels. Thus, HDL and triglyceride levels suggest lower risks of coronary heart disease for black men. The per-unit risk of elevated Lp(a) is less in blacks than whites, suggesting that Lp(a) interacts with other metabolic factors in blacks (Marcovina et al., 1993). If Lp(a) inhibits plasminogen, it might elevate black risks of stroke (Shintani et al., 1993). If Lp(a) increases cholesterol uptake in atheromas, this suggests interactions with cholesterol—an effect that could be dampened because black males have lower LDL and higher HDL levels. Thus, Lp(a) and hypertension may explain the higher mortality from strokes

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--> for blacks than whites in middle and late-middle ages. Since Lp(a) has genetic determinants, and mortality selection has been shown in a number of twin studies to eliminate elevated genetic risks of mortality from coronary heart disease by age 85 (e.g., Marenberg et al., 1994; Carmelli et al., 1994; Reed et al., 1991; Heller et al., 1993), these age patterns of disease risk (and mortality selection) could contribute to a convergence of mortality patterns in blacks and whites owing to a different age dependence of circulatory diseases related to atherosclerosis at late ages. Apo E is important in circulatory disease and dementia. One study suggested that the effects of Apo E differ in men and women (Ferrières et al., 1994). In some studies, Apo E2 and E4 subtypes lowered Lp(a), a fact significant for black circulatory disease risks. E2 was associated with reduced, and E4 with elevated, risks of heart disease (Tiret et al., 1994). E2 was associated with higher stroke risks—possibly interacting with diabetes (Couderc et al., 1993). The effects of E2 were stronger in postmenopausal females (Schaefer et al., 1994), lowering LDL twice as much as for premenopausal females. Racial differences in atherosclerosis are also evaluated by studying circulatory pathologies in African Americans and whites. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY, 1993) study collected material on thoracic and abdominal aortas and right coronary arteries in 1,532 autopsied black and white, male and female, subjects aged 15 to 34 for 1987 to 1990. PDAY did not show more coronary artery raised lesions in white, than black, males. This differed from the International Atherosclerosis Project (Guzmán et al., 1968) and other earlier studies (Strong and McGill, 1963; Eggen and Solberg, 1968). In autopsies of 1,243 blacks and whites aged 30 to 69 in New Orleans (Eggen et al., 1965) and in the International Atherosclerosis Project, where 23,000 autopsies from 15 geographic locations and four race-sex groups were assessed (Strong, 1972), there was less calcification of atheromas in blacks than in whites. Strong concluded that race differences were due to such factors as diet, activity, smoking, and stress. One dietary factor could be vitamin D consumption and age differences in its metabolism and its effects on calcium. The New Orleans study of autopsies from the 1950s to the 1960s suggested that atherosclerosis was 10 years of age more advanced in whites than in blacks. Differences between the findings of PDAY and the International Atherosclerosis Project may be due to recent decreases in the prevalence of atheromas in white males and a stable prevalence in black males. Diabetes Mellitus (Adult Onset) There are two types of diabetes mellitus. One, juvenile onset, is due to the autoimmunological destruction of pancreatic cells that produce insulin. Here we examine adult onset diabetes mellitus, which is not insulin dependent but is

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--> Complete Table on previous page. Third, we examined the linkage of disability with mortality at late ages. In a model describing the interaction of disability and mortality, there was a more rapid increase in mortality with age for whites than for blacks. This occurred for both males and females and was consistent with the higher disability found in

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--> blacks at later ages. The age at crossover in the NLTCS data was similar to ages found in extinct cohort analyses of death certificate data and Kestenbaum's (1992) matched record study. Thus, we were able to examine three data elements (age trajectory of morbidity, mortality-morbidity linkages, and disability-mortality linkages) to develop a picture of U.S. racial differences in the age dependence of mortality, morbidity, and disability to extreme ages. References Aronson, M.K., W.L. Ooi, H. Morgenstern, A. Hafner, D. Masur, H. Crystal, W.H., Frishman, D. Fisher, and R. Katzman 1990 Women, myocardial infarction, and dementia in the very old. Neurology 40:1102-1106. Ayanian, J.Z. 1994 Race, class, and the quality of medical care. Journal of the American Medical Association 271(15):1207-1208. Barker, D.J.P., K.M. Godfrey, C. Osmond, and A. Bul 1992 The relation of fetal length, ponderal index and head circumference to blood pressure and the risk of hypertension in adult life. Pediatric and Perinatal Epidemiology 6:35-44. Barker, D.J.P., T.W. Meade, C.H.D. Fall, A. Lee, C. Osmond, K. Phipps, and T. Stirling 1992 Relation of fetal and infant growth to plasma fibrinogen and factor VII concentrations in adult life. British Medical Journal 304:148-152. Becker, T.M., C.M. Wheeler, N.S. McGough, C.A. Stidley, C.A. Parmenter, M.H. Dorin, and S.W. Jordan 1994 Contraceptive and reproductive risk for cervical dysplasia in Southwestern Hispanic and non-Hispanic white women. International Journal of Epidemiology 23(5):913-922. Bild, D.E., A. Fitzpatrick, L.P. Fried, N.D. Wong, M.N. Hann, M. Lyles, E. Bovill, J.F. Polak, and R. Schulz 1993 Age-related trends in cardiovascular morbidity and physical functioning in the elderly: The cardiovascular health study. Journal of the American Geriatrics Society 41:1047-1056. Boult, C., R.L. Kane, T.A. Louis, and J.G. Ibrahim 1991 Forecasting the number of future disabled elderly using Markovian and mathematical models. Journal of Clinical Epidemiology 44:973-980. Bowden, M., J. Crawford, H.J. Cohen, and O. Noyama 1993 A comparative study of monoclonal gammopathies and immunoglobulin levels in Japanese and United States elderly. Journal of the American Geriatrics Society 41:11-14. Browner, W.S., A.R. Pressman, M.C. Nevitt, J.A. Cauley, and S.R. Cummings 1993 Association between low bone density and stroke in elderly women: The study of osteoporotic fractures. Stroke 24:940-946. Browner, W.S., D.G. Seeley, T.M. Vogt, and S.R. Cummings 1991 Non-trauma mortality in elderly women with low bone density. Lancet 338:355-358. Campbell, A.J., W.J. Busby, and C. Robertson 1993 Over 80 years and no evidence of coronary heart disease: Characteristicsof a survivor group . Journal of the American Geriatrics Society 41:1333-1338. Carmelli, D., D. Robinette, and R. Fabsitz 1994 Concordance, discordance and prevalence of hypertension in World War II male veteran twins. Journal of Hypertension 12:323-328.

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