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Page 99 5 Extent and Distribution of Chronic Disease: An Overview There are subtle, but important, differences between health and the absence of disease and between health promotion and disease prevention. The Constitution of the World Health Organization states in its preamble that "health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Definitions of health and of disease prevention promulgated by the Office of Disease Prevention and Health Promotion of the U.S. Department of Health and Human Services (DHHS) stress the differences in terms of personal behavior, level of prevention, and sense of well-being: Health promotion = personal, environmental, or social interventions that facilitate behavioral adaptations conducive to improved health, level of function, and sense of well-being. Disease prevention = personal, environmental, or social interventions that impede the occurrence of disease, injury, disability, or deathor the progression of detectable but asymptomatic disease (J. Michael McGinnis, DHHS, personal communication, 1988). The committee carefully considered these definitions and decided that any attempt to address the association between diet and health in its broadest sense would necessarily be superficial, incomplete, and so diffuse as to be ineffective. Thus, it opted to focus on specific diet-related chronic diseases and conditions related to them. The definition of diet is straightforward: Diet comprises all food and drink consumed by people. It is characterized by the average and the distribution of nutrients and foods consumed by an individual or by a defined group. The committee gave special attention to major diet-related chronic diseases and conditions of adulthood, including atherosclerotic cardiovascular diseases (i.e., coronary heart disease, stroke, and peripheral arterial diseases), hypertension and related diseases, obesity and related diseases, cancers, osteoporosis, diabetes mellitus, hepatobiliary disease, and dental caries. It selected these because, according to current evidence, they are the most common diet-associated causes of death and disability among U.S. adults. This chapter presents the descriptive epidemiologic features of those eight chronic diseases and conditions. Atherosclerotic Cardiovascular Diseases Coronary Heart Disease Coronary heart disease (CHD) affects the cardiac muscle, mainly as a result of atherosclerotic disease of the coronary arteries and its complications. Atheromas and thrombosis combine to interrupt blood flow to the heart, producing clinical
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Page 100 FIGURE 5-1 Rate of deaths from CHD per 100,000 population among 35- to 74-year-old men in 1977 (except as otherwise noted) by country. Adapted from the report of the Inter-Society Commission for Heart Disease Resources (1984). events that may include sudden death. Morbidity from CHD, measured by population-based surveys and hospital records, includes clinical syndromes of myocardial infarction with damage to and scarring of the myocardium; coronary insufficiency, including angina pectoris and other symptoms of inadequate blood supply; complex arrhythmias, which may lead to sudden coronary death; and chronic heart disease characterized by heart failure or arrhythmias. Mortality from CHD is defined as the number or proportion of death certificates that are coded as International Classification of Disease (ICD) categories 410-411 (myocardial infarction) or 412-414 (angina pectoris and other chronic heart disease manifestations). Population Differences In Frequency Among Countries Figure 5-1 depicts wide differences among countries in the vital statistics on CHD death among 35- to 74-year-old men in the 1970s. The highest reported CHD death rates occurred in Finland and the English-speaking countries, including the United States; the lowest rates were in Japan (Inter-Society Commission for Heart Disease Resources, 1984). CHD death rates for women in the same year (not shown) were highest in Northern Ireland, Scotland, and the United States and lowest in Japan (Inter-Society Commission for Heart Disease Resources, 1984). These large geographic differences in CHD death rates were confirmed by studies comparing geographic differences in CHD incidence rates, such as the Seven Countries Study, in which the 10-year incidence rate among men 40 to 59 years old at the beginning of the study was about 200 per thousand in Finland as compared to about 40 per thousand in Japan and the Greek Islands (Keys, 1980). Geographic differences in trends of reported deaths from CHD have been equally dramatic (see Figure 5-2). The largest decline among men from 35 to 74 years old occurred in the United States, followed closely by Australia and Canada, whereas rates rose strongly in Northern Ireland, Poland, and Bulgaria. Similar changes in death rates were also reported for women (not shown)the largest
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Page 101 FIGURE 5-2 Percent change in rates of death from CHD from 1969 through 1977 among 35- to 74-year old men by country. Adapted from the report of the Inter-Society Commission for Heart Disease Resources (1984). declines again occurring in the United States and Australia, smaller decreases in other countries, and increases in several Eastern European countries (Inter-Society Commission for Heart Disease Resources, 1984). Within the United States In the United States, there are substantial regional differences in CHD death rates. In 1980, rates were highest in the East and Southeast (290-305 deaths per 100,000), intermediate (210-249) in the Midwest, and lowest (149-209) in the West and Southwest (DHHS, 1987). Time Trends in the United States From the 1950s to the mid-1960s, CHD rates in the United States rose 1 to 2% per year among men and women, whites and nonwhites. Subsequently, death rates declined by 2 to 3% per year. This decline has affected all ages, but has been especially evident in younger groups and was observed a few years earlier in women than in men. From 1973 through 1979, CHD death rates again increased, but since 1980, they have returned to the 1965-1973 rate of decline. Unadjusted data suggest that the decline has continued through 1986 and early 1987, but with a slowing of rate (DHHS, 1987). This decline was greater in better educated, more affluent groups (DHHS, 1987) and is characterized by fewer out-of-hospital deaths, sudden unexpected deaths, and acute nonfatal myocardial infarction (Anastasiou-Nana et al., 1982; Elveback et al., 1986; Folsom et al., 1987; Gillum et al., 1984; Goldberg et al., 1986; Goldman et al., 1982; Gomez-Marin et al., 1987; Kuller et al., 1986; Pell and Fayerweather, 1985). These findings have been attributed to the increased availability of more sophisticated cardiac care and more effective emergency services (Gillum et al., 1984; Goldman and Cook, 1984). In addition, the decline in CHD deaths was generally accompanied by, and probably preceded by, decreased CHD incidence and by lowered average levels of factors associated with increased CHD risk in the population (e.g., cigarette smoking, hypertension, and high serum cholesterol levels) (Inter-Society Commission for Heart Disease Resources, 1984;
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Page 102 Pell and Fayerweather, 1985). A decline in severity of atherosclerotic lesions at autopsy has also been noted (Solberg and Strong, 1983), although current evidence is insufficient to link this to the concomitant decrease in CHD mortality rates. Similarly, in long-term cohort studies of CHD, decreases in sudden and out-of-hospital deaths, in-hospital proportion of cases dying (case fatality), and discharge diagnoses of CHD have been reported (Inter-Society Commission for Heart Disease Resources, 1984). The decrease in CHD case fatality rates may reflect improved medical care. With the exception of an increased incidence of nonfatal myocardial infarction noted in a study of women in Rochester, Minnesota (Elveback et al., 1981), there is much evidence that the incidence of first coronary events is declining (Kuller et al., 1986; Pell and Fayerweather, 1985). The evidence for improved survival from myocardial infarction. over the short term (30 days) is strong (Folsom et al., 1987; Goldberg et al., 1986; Pell and Fayerweather, 1985), but not consistent (Elveback et al., 1986; Goldman et al., 1982). One study has shown an improvement in 4-year survival after myocardial infarction, but much of that was due to improved survival in hospital (Gomez-Marin et al., 1987). In the United States, there have been large regional differences in the trends of CHD death rates between 1960 and 1980 (DHHS, 1987). For example, age- and sex-adjusted CHD mortality rates (ages 35 to 74) declined 48 to 53% in Maryland, Delaware, Illinois, and Nevada and 40 to 44% in Connecticut, Washington, and California. Smaller declines have been noted throughout the western, midwestern, southern, and south-central states including Appalachia. The smallest changes were observed in Oklahoma, Mississippi, Tennessee, and Kentucky, where there were declines of only 12 to 21%. Associations Between Risk Factors in Individuals and CHD Age CHD prevalence, incidence, and mortality rates rise steeply with age, approximately doubling in each 5-year age class past age 24. The decline in age-specific CHD death rates between 1968 and 1978 in the United States occurred across all age groups; it was 40 to 50% for those in the 35- to 44-year-old age group and 15 to 20% among those over age 70 (DHHS, 1987). Sex CHD death rates in men are three times greater than in women in such high-incidence countries as the United States, the United Kingdom, northern European countries, New Zealand, and Australia (Inter-Society Commission for Heart Disease Resources, 1984). These sex differences are smaller after women pass menopause and in such low-CHD-incidence countries as France and Japan. In countries where CHD deaths have declined; percentage declines have generally been steeper among women than among men. Ethnic, Racial, and Migrant Differences Ethnic and racial differences in CHD deaths within countries are closely associated with socioeconomic level. In the United States, CHD death rates are highest for white males, followed in descending order by black males, other nonwhite males, black females, white females, and nonwhite (other than black) females. The greatest rate of decline in CHD deaths between 1968 and 1978almost 50%occurred among nonwhite (but not black) women, followed by white women. Black women had the smallest decline (DHHS, 1987). Differences among migrants were systematically documented in the Ni-Hon-San study conducted among Japanese living in Japan, Honolulu, and San Francisco. In that study, investigators observed that CHD prevalence and incidence rates tripled among Japanese within a generation of their migration to the West Coast of the United States and doubled in Japanese who migrated to Hawaii (Marmot et al., 1975; Robertson et al., 1977). This change was generally paralleled by changes in average levels of risk factors, including saturated fat in the diet and serum cholesterol levels. Similar changes occurred in Boston men who were born in Ireland compared to their brothers who stayed in Ireland (Kushi et al., 1985) and in South Pacific islanders who settled in New Zealand (Beaglehole et al., 1977; Prior and Stanhope, 1980). In all these groups, rates among migrants were near those of the newly adopted culture within 10 to 20 years. Socioeconomic, Occupational, and Psychosocial Factors - The relationship of socioeconomic class and occupation to CHD risk differs among cultures. For example, a social classification based primarily on occupation was positively associated with CHD
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Page 103 mortality in the United Kingdom in the 1950s and 1960s. Since 1960, this picture has changed; the social classification is now inversely related to CHD deaths in England and Wales (Marmot et al., 1978). In the United States, hourly wage earners now have greater CHD mortality and incidence rates than do salaried employees, although there appear to be no specific occupational exposures that exacerbate CHD risk (Pell and Fayerweather, 1985). Other relationships are found between psychosocial factors and CHD risk. Generally, better educated people are nonsmokers and have healthier patterns of eating, lower serum cholesterol levels, leaner body mass index, and greater physical activity. Numerous studies have indicated slight to moderately strong associations between CHD risk and other psychosocial and behavioral characteristics, but the existence of coronary-prone behavior and personality has been increasingly questioned because few of those studies controlled for social networks, physical activity, diet, and alcohol intake (Inter-Society Commission for Heart Disease Resources, 1984; Jenkins, 1983). Familial and Genetic Factors Family history of early-onset CHD is an independent risk indicator in high-risk populations (Inter-Society Commission for Heart Disease Resources, 1984); however, familial hypercholesterolemia accounts for only a small percentage of the people with relatively high serum cholesterol levels in affluent cultures. It is likely that individual differences in biologic risk factors such as serum lipoprotein levels and in responses to dietary factors (e.g., dietary cholesterol) are determined in large part by genetic factors. However, the absence of specific genetic markers limits the power of family studies to separate the genetic components. New findings concerning cell receptors for lipoproteins hold promise for improving understanding of the differences in individual responses to diet and susceptibility to CHD. Other Risk Factors The relationship of specific dietary components to serum lipoprotein levels is discussed throughout this report (e.g., Chapters 6-10, 14, 16, 17, and 19), as are relative risk, attributable risk, and the population risk attributable to elevated blood lipoproteins. CHD is a classic model of a disease with multiple causes. Evidence indicates that a diet high in saturated fatty acids and cholesterol along with relatively high levels of serum cholesterol are the greatest contributors to elevated population risk of atherosclerosis and CHD; population risk differences are largely explained by these related factors. However, within populations with a significant burden of atherosclerosis, several factors interact to determine an individual's risk. The most prominent of these, after age, sex, diet, and blood lipoproteins, are the level of arterial blood pressure and the number of cigarettes smoked. Peripheral arterial disease is one of the strongest independent predictors of CHD, stroke, and all causes of death (Criqui et al., 1985a). Numerous other factors, including lack of habitual physical activity, relative body weight (see section below on Obesity and Related Diseases), and diabetes, contribute to CHD (Inter-Society Commission for Heart Disease Resources, 1984). Stroke Stroke is the abrupt onset of neurological disability due to infarction of the area of brain served by an artery that is clogged by atherosclerotic plaque, blocked by an embolus, or ruptured, with destruction of brain tissue by hemorrhage. Transient ischemic attacks (TIAs) are episodes of temporary neurological disability due to insufficient arterial blood supply to the brain. In the United States, most strokes result from cerebral infarction, followed in frequency by the two major forms of cerebral hemorrhageintracerebral and subarachnoid. Stroke is a major cause of death among adults worldwide. In industrial countries, it is usually third among causes of death, following heart diseases and cancer. Population Differences in Frequency Among Countries There are large differences in reported mortality rates for stroke. For example, age-adjusted 1970 estimates of prevalence rates for stroke per 100,000 people were 556 in Rochester, Minnesota, and 363 in the United Kingdom (Kurtzke, 1976). Studies in Japan suggest that the distribution of the types of stroke (e.g., infarction and hemorrhage) also varies widely (Omae et al., 1976). In populations, death rates from cerebral infarction generally parallel those from atherosclerosis and CHD, whereas rates of intracerebral hemorrhage usually parallel the frequency of hypertension. For example, stroke
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Page 104 is the leading cause of deaths among adults in Japan, where hypertension is prevalent but CHD is uncommon (Komachi, 1977). In past years, accurate assessment of stroke incidence and mortality has been hampered by frequent misdiagnosis. The descriptive epidemiology of stroke should improve, however, as diagnosis is enhanced by computed tomography (CT), which allows differentiation among the several basic causes of the stroke syndrome. Within the United States Strokes of all types were reported as the cause of death for approximately 182,000 persons in the United States in 1977; limitations in death certification do not permit reliable estimates by type of stroke. The American Heart Association (AHA, 1983) estimated the 1981 prevalence of residual damage from strokes at 1.87 million and of coronary disease at 4.6 million. Fatality shortly after the stroke occurs in about 15% of those affected, another 16% require institutional care, and 50% are permanently disabled (Kannel and Wolf, 1983). The average annual incidence of stroke in a 20-year follow-up of 45- to 74-year-old subjects in Framingham, Massachusetts, was 340 per 100,000 among men and 290 among women. Two-thirds of these cases had cerebral infarction (Kannel and Wolf, 1983). Rates were about equal for men and women from age 65 onward, and the rates climbed precipitously with age1 per thousand at ages 45 to 54, 3.5 at ages 55 to 64, 9.0 at ages 65 to 74, 20.0 at ages 75 to 84, and 40.0 at age 85 and over. In the United States, approximately 50% of the strokes are attributed to atherosclerosis and thrombosis, 12% to cerebral hemorrhage, 8% to subarachnoid hemorrhage, and 8% to embolism. The remainder are ill-defined (Kurtzke, 1976). Time Trends in Mortality and Morbidity Stroke deaths have declined for the past 50 years. In the 1940s and 1950s the rate of decline was 1% per year. Since 1972, the rate of decline has increased to 5% per year (Levy, 1979; Soltero et al., 1978). Between 1968 and 1981, the age-adjusted death rate from stroke fell 46% (Inter-Society Commission for Heart Disease Resources, 1984). The decline has been especially notable among nonwhites, especially nonwhite females. Population-based data on stroke incidence in the United States are rare, but in Rochester, Minnesota, the average annual incidence for all types of stroke declined from 190 per 100,000 during 1945-1949 to 104 during 1970-1974 (Garraway and Whisnant, 1987; Garraway et al., 1979). The Rochester data also documented that the decline in death rates ascribed to intracerebral hemorrhage began well before better diagnoses became possible through the use of more widely available CT scans and continued to 1979. There is evidence that fatality among hospitalized stroke patients has not declined much. This indicates that the drop in deaths overall is attributable to out-of-hospital stroke deaths and suggests strongly that incidence must therefore have declined (Gillum et al., 1985). The underlying causes of the long-term decline in stroke deaths are not well established. It is clear, however, that there has been improved control of the major risk factorhypertensionas well as effective prevention of stroke in cases experiencing TIA. Nevertheless, computer modelling by Bonita and Beaglehole (1986) suggests that drug treatment of hypertension contributed less to reduced stroke mortality than reduction in levels of population risk factors (e.g., serum cholesterol). Associations Between Risk Factors in Individuals and Stroke Age Stroke deaths and incidence rates are very low until age 45. After that, they rise precipitously, more than doubling for each decade (Kannel and Wolf, 1983). Sex Stroke deaths, prevalence, and incidence rates are generally similar for men and women after age 55, in contrast to the much larger and more persistent sex differential for CHD. Cerebral atherosclerosis and stroke begin later in life. In postmenopausal women this is presumed to be due to the loss of protection afforded by their hormonal status (Kannel and Wolf, 1983). The downward trend in stroke deaths, which started earlier and was greater among women, can be explained in part by more effective hypertension control (Garraway and Whisnant, 1987). Ethnic, Racial, and Migrant Differences In the United States, stroke deaths and incidence rates are higher among blacks than among whites (Kannel and Wolf, 1983). However, Ni-Hon-San data suggest that environment exerts an even greater influence, since stroke rates were substantially greater among Japanese living in Japan than among Japanese migrants living in Ha-
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Page 105 waii and California (Kagan et al., 1976, 1980). Because there is little difference in the prevalence of hypertension in migrant Japanese populations, the difference in stroke rates was an early clue to the possibility that habitual diet and serum cholesterol levels play a role in hemorrhagic stroke (Kagan et al., 1976; Komachi, 1977; Takeya et al., 1984; Ueshima et al., 1980). Other studies confirm the role of acculturation in the rise and fall of stroke risk (Bonita and Beaglehole, 1982). Socioeconomic, Occupational, and Psychosocial Factors There are few systematic data on the relationship of socioeconomic, occupational, or psychosocial characteristics to stroke death or incidence. Familial and Genetic Factors Close relatives of a stroke patient are at slightly greater risk of stroke than genetically unrelated persons (Heyden et al., 1969). Results of a study conducted in Göteborg, Sweden (Welin et al., 1987), suggest that maternal history is more important than paternal history in determining risk. Other Risk Factors Hypertension has been consistently, strongly, continuously, and independently related to risk of stroke in individuals within populations at high risk for stroke (Dyken, 1984; Kannel and Wolf, 1983; Welin et al., 1987). Because of the great prevalence of hypertension in the United States, the population risk of stroke attributable to hypertension, as well as the risk for stroke for individuals, is high. The risk associated with elevated blood pressure increases continuously with increases in diastolic and systolic levels. It increases with increases in systolic blood pressure levels even when the diastolic level remains constant. In the Framingham 24-year follow-up study, for example, the 2-year incidence of stroke among men and women ages 50 to 79 was progressively greater as systolic blood pressure levels increased from below 140 to above 160 mm Hg, regardless of level of diastolic pressure. This finding suggests that an elevated systolic blood pressure even in the presence of normal diastolic blood pressure (i.e., isolated systolic hypertension) constitutes a risk for stroke (Kannel and Wolf, 1983). Age-adjusted annual incidence of cerebral infarction was more than twice as great in people with diabetes as in those without the disease (Kannel and Wolf, 1983). This differential applied to both sexes and was independent of the associated risk factors: blood pressure, serum cholesterol, cigarette smoking, and electrocardiographic findings. Cigarette smoking was positively and independently associated with cerebral infarction in men below age 65 in the Honolulu and Framingham studies (Abbott et al., 1986; Kannel and Wolf, 1983), but only a weak relationship was found in the Chicago Stroke Study (Ostfeld et al., 1974). In the Framingham Study, stroke incidence was negatively related to relative body weight in men over age 65, but positively related under age 65 (Kannel and Wolf, 1983). Excessive abdominal fat was positively related in Göteborg men (Welin et al., 1987). Several surveys link self-reported alcohol intake to risk of stroke, including cerebral hemorrhage and cerebral infarction. Age-adjusted incidence rose steadily from the level of nondrinkers to those drinking more than 30 ounces of alcohol per month in populations followed in Japan (Omae et al., 1976), Honolulu (Kagan et .al., 1980), Alabama (Peacock et al., 1972), Framingham (Marshall, 1971), and Chicago (Gill et al., 1986). The presence of CHD, peripheral arterial disease (PAD), or hypertensive heart disease is strongly associated with stroke risk (Ostfeld et al., 1974). Peripheral Arterial Disease (PAD) The term PAD is used here to refer to a specific entity of peripheral vascular disease (PVD) and includes clinical syndromes of arterial insufficiency in the lower extremities. These syndromes are characterized by pain, inflammation, and ischemic damage to soft tissues from occlusion of the arteries. The characteristic syndrome of PAD is intermittent claudicationi.e., cramping, aching, and numbness of the extremitieswhich is induced by exercise but resolves promptly when exercise ceases. Arterial aneurysms, an advanced form of PAD, lead to swelling, tissue separation, or rupture of major arteries in the abdomen or pelvis. Arteriosclerosis obliterans is the most common clinical form, constituting the majority of cases of public health concern. Its basic pathology is obliteration of the arterial lumen due to the formation of atherosclerotic plaques with or without thrombosis. PAD is diagnosed by a combination of clinical history (e.g., history of pain in the extremities upon exertion) and changes in the color, temperature, and appearance of the skin; arterial pulsations or abnormalities of blood flow; and blood pressure or pulse transmission or reappearance
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Page 106 time. Angiography is the reference method for assessing type and severity of the arterial disease, but ultrasound promises to provide effective, noninvasive diagnoses. There are few systematic data for comparing frequency of PAD among or within populations, and few studies of risk characteristics have been conducted within populations. In addition, mortality data for PAD are unreliable because of the variety of syndromes involved, their low relative frequency as a direct cause of death, and uncertainties pertaining to cause of death, which is usually ascribed to associated cardiac, brain, or kidney disease. Furthermore, there is no reliable information on trends in prevalence, incidence, or deaths from PAD. An exception is one population-based study, predominantly of whites with an average age of 66, which provided evidence that large-vessel PAD was present in 11.7% of the subjects (Criqui et al., 1985b). Peripheral venous disease is not considered here because of its remote relationship to diet and nutrition. Associations Between Risk Factors in Individuals and PAD Age PAD is characteristically, but not exclusively, a disease of older age. In a California study, there was a dramatic increase in PAD prevalence by age (Criqui et al., 1985b). Framingham data also showed a steady rise in the average annual incidence of intermittent claudication by age, mainly from age 55 onward (Kannel and McGee, 1985). Clinical onset may be delayed to older ages by the large caliber of the arteries involved and, thus, the extreme degree of obstructive atherothrombotic disease that is required before blood flow is sufficiently impaired to produce symptoms. Sex There are few systematic data on the distribution of PAD by sex. An older Mayo Clinic series conducted in the 1940s indicated that the prevalence of PAD was six times higher in males than in females (Allen et al., 1946). In California, the prevalence of intermittent claudication was greater in men (2.2%) than in women (1.7%) (Criqui et al., 1985b). In Framingham, the incidence of intermittent claudication in men was approximately twice that in women up to age 65 (11.6 vs 5.3%); at older ages, the incidence was similar (Kannel and McGee, 1985). Ethnic, Racial, and Migrant Differences There are no systematic population data on ethnic, racial, and migrant differences in PAD, but a clinical series in the United States suggest no large ethnic or racial differences (Juergens et al., 1959). Socioeconomic, Occupational, and Psychosocial Factors Systematic data are not available. Familial and Genetic Factors There is apparently no strong familial or genetic role in PAD. However, diabetes mellitus, which is associated with PAD as described below, does aggregate in families and could thus lead to a similar familial association for PAD. Other Risk Factors Clinical observations suggest a strong concentration of PAD risk among people with diabetes (Schadt et al., 1961). This was confirmed by the greater annual incidence of intermittent claudication in diabetic men and women in the Framingham Study. The attributable fractioni.e., the excess cases of intermittent claudication due to diabetes (at ages 45 to 74)affects more men (13.6%) than women (2.7%) (Kannel and McGee, 1985). Elevation of blood sugar, urinary sugar, or clinical diabetes increases the risk for intermittent claudication about four- or fivefold. In a population-based cohort of diabetics in Rochester, Minnesota, the cumulative incidence of PAD was 15% at 10 years and 45% at 20 years after diagnosis of diabetes (Melton et al., 1980). Diabetes and glucose intolerance are consistently associated with PAD in these and other studies (Bothig et al., 1976; Keen et al., 1965; Reunanen et al., 1982). The incidence of intermittent claudication increases steadily and steeply at all ages with the number of cigarettes smoked (Kannel and McGee, 1985). Even beyond age 65, women smokers in Framingham were at greater risk. Some clinical series some years ago indicated that 90% of all PAD cases were cigarette smokers (Juergens et al., 1960). The strong relationship of PAD to smoking was confirmed by autopsy studies in which the incidence of aortic atheromatous plaque in white males was much greater in smokers than in nonsmokers (Strong and Richards, 1976).
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Page 107 The relationship between systolic blood pressure and annual incidence of intermittent claudication in the Framingham 14-year followup was positive in both sexes. Ratios between hypertensives and normotensives were 2 or 3 to 1 (Kannel and Sorlie, 1979). In the Framingham study, there was an inverse relationship between physical activity and intermittent claudication, but it was not statistically significant (Kannel and Sorlie, 1979). In Framingham, there was also a strong curvilinear relationship between the incidence of intermittent claudication and a coronary risk index of CHD risk characteristics including age, blood cholesterol level, electrocardiographic (ECG) findings, systolic blood pressure, relative weight, hemoglobin, and cigarette use (Kannel and McGee, 1985). The strongest relationships were observed for cigarette smoking and hypertension for both sexes and for impaired glucose tolerance, which was stronger for women than for men. Serum total cholesterol and relative weight were only weakly significant risk factors. Clustering of intermittent claudication with other atherosclerotic and cardiovascular diseases was also pronounced in the Framingham Study. Overt coronary disease, cerebrovascular disease, or congestive heart failure was found in one out of three cases of intermittent claudication at the time it was initially diagnosed, suggesting common risk characteristics. The relative risk of developing intermittent claudication in Framingham patients with CHD was four times the standard risk in the cohort, whereas people with angina pectoris had three times greater risk (Kannel and Shurtleff, 1971). In the most recent systematic study of multiple risk factors for PAD, Criqui used objective diagnostic criteria for large- and small-vessel diseases (Michael Criqui, University of California, San Diego, personal communication, 1988). For large-vessel disease, they showed that age, smoking, fasting plasma glucose, and systolic blood pressure were strongly associated with the prevalence of PAD and that obesity, LDL, and HDL were marginally related. Small-vessel PAD was only weakly related to atherosclerotic cardiovascular disease risk factors. In general, the risk factors for PAD are similar to those for CHD and stroke, although their relative importance differs. For example, diabetes and smoking are the preeminent risk factors for PAD but not for CHD, followed by triglycerides, VLDL, and blood glucose tolerance, and to a lesser extent LDL, HDL, and serum total cholesterol, which strongly predict CHD. Hypertension and Hypertension-Related Diseases Hypertension is defined as elevated arterial blood pressure measured indirectly by an inflatable cuff and pressure manometer. Blood pressure is a continuous or graded phenomenon, and .the risk of hypertension increases steadily with blood pressure leveleither systolic (SBP) or diastolic (DBP). Therefore, any definition of elevated blood pressure is arbitrary and is done primarily to facilitate decisions regarding pharmacological therapy. Traditionally, physicians diagnose hypertension using DBP, which is the lower value found during the resting phase of the cardiac cycle. DBP levels have been closely associated in clinical studies with manifest diseases or complications associated with high blood pressure (e.g., stroke, hypertensive heart disease, CHD, and kidney disease) and are used as the basis of most treatment decisions. Systematic population studies indicate, however, that systolic blood pressure, the higher value recorded during cardiac systole, is not only a more reliable measurement but also a more precise indicator of the risk of future complications in hypertension. For practical treatment purposes and for population comparisons, the following criteria developed by the World Health Organization (WHO, 1978) are often used: normotension, systolic £ 140 and diastolic £ 90 mm Hg; borderline hypertension, systolic 141-159 and diastolic 91-94 mm Hg; and hypertension, systolic ³160 and diastolic ³ 95 mm Hg. Severe hypertension is often defined as diastolic levels of 115 mm Hg and above. The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (NC, 1988) added classifications for high normal, mild, moderate, severe, and isolated systolic hypertension (see Table 20-1, Chapter 20). Deaths related to hypertension have been variously classified over recent years. They have either been considered as a separate entity or combined with such classes of atherosclerotic cardiovascular diseases as CHD and stroke. Thus, it is not useful to consider vital statistics alone in discussing the epidemiology of hypertension. Hypertension is treated here primarily as a risk characteristic for atherosclerotic cardiovascular diseases rather than as a disease entity in itself.
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Page 108 Population Differences in Blood Pressure and Hypertension Among Countries Surveys comparable to those of the U.S. National Center for Health Statistics (DHEW, 1963) have not been conducted outside the United States. However, many smaller-scale surveys attest to the fact that hypertension is prevalent in industrialized nations throughout the world. The prevalence in England (Hamilton et al., 1954), Western Europe (Keys, 1980), and Australia (MacMahon and Leeder, 1984) is similar to that in the United States. Data from China (Wu et al., 1982), Japan (Komachi and Shimamoto, 1980), and Korea (Kesteloot et al., 1976) show prevalence rates in urban populations equal to or greater than those in United States. A low prevalence of hypertension has often been found in studies of traditional rural populations outside Western culture. More than 20 societies, representing a variety of races, diets, habitats, and modes of life, have been found to have virtually no hypertension and little or no tendency for blood pressure to rise with age. Social and anthropological characteristics of these populations are similar: they are relatively isolated, subsistence cultures; their salt intake is less than 4.5 g daily; there is an absence of obesity; and they remain physically active throughout life (Page, 1979). For more detailed data on the geographic distribution of blood pressure, see Epstein and Eckoff (1967). Within Countries There have been reports of regional differences in the frequency of hypertension and in mean blood pressure values. People in the southeastern United States tend to have higher pressures (DHHS, 1986) as do people in the northern provinces of Japan (Komachi, 1977; Omae et al., 1976) and in the French-speaking areas of Belgium (Kesteloot et al., 1980). Regional differences are not well explained, but they appear to be independent of race and socioeconomic status. Time Trends in Frequency and Mortality In the United States, average trends in blood pressure for people between the ages of 25 and 74 have been examined in surveys conducted by the National Center for Health Statisticsthe Nationwide Health Examination Survey (NHES I) of 1960-1962 (DHEW, 1963) and the Nationwide Health and Nutrition Examination Surveys of 1971-1975 (NHANES I) (Abraham et al., 1983) and 1976-1980 (NHANES II) (Carroll et al., 1983). Assuming comparability of methods and design (DHEW, 1963; DHHS, 1986), one can see no significant trend in the population means or the distribution of average blood pressures for given ages between the first two surveys. However, the third survey, NHANES II, shows markedly lower average systolic blood pressures at all ages above 30. A much lower prevalence of hypertension is also apparent in people over 40 in that survey compared to those in the earlier two. When NHANES II data (DHHS, 1986) are used, the prevalence of definite hypertension is 17.7% in adults as defined by the World Health Organization (WHO, 1978) or 29.7% as defined by the criteria of the third Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC, 1988). Concurrent with the decline in hypertension prevalence and in mean blood pressure indicated in these U.S. national surveys, there has been an improvement in the status of medical detection and control of high blood pressure. Previously undetected hypertension (i.e., cases newly diagnosed at screening) was halvedfrom 51.1% during 1960-1962 to 26.6% during 1976-1980. The proportion of hypertension controlled by medication doubledfrom 16% during 1960-1962 to 34.1% during 1976-1980. Data are insufficient to attribute these changes with certainty to medical detection and control or to primary prevention in the general population. Both have occurred as modelled by Bonita and Beaglehole (1986), but there is as yet no direct evidence of a decrease in mean population blood pressure independent of medical treatment. There is also evidence that trends in high blood pressure are not an indirect result of changes in average relative weight or alcohol intakeboth of which have risen in recent years in the United States while mean blood pressure has fallen. The increased risk of morbidity and mortality from cardiovascular diseases associated with hypertension has been repeatedly demonstrated in epidemiologic studies throughout the industrialized world (Stamler et al., 1975). The risk of hypertension varies markedly with age, sex, race, and the total burden imposed by associated risk factors, including socioeconomic status, occupation, obesity, family history, psychosocial stresses, and other factors (as discussed below). The American Heart Association (AHA, 1973) has published multiple risk calculations for different age and sex
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Page 109 groups based on major risk factors using Framingham study data. In general, the risk for major coronary disease events increases by 30% for each 10 mm Hg increase in systolic blood pressure in both men and women of all ages (Dawber and Kannel, 1972). Interaction of hypertension with other risk factors may alter their risk as much as sixfold. A striking feature of the epidemiology of hypertension is the remarkable decrease in hypertension-related deaths, i.e., from all cardiovascular disease, cerebrovascular disease, renal disease, hypertensive heart disease, and CHD (DHHS, 1987). This trend is so consistent and strong that it must represent a real change, independent of improved classification in death certification. The beginning of the decline in hypertension-related mortality clearly antedated the widespread use of effective antihypertensive drugs, but it accelerated in the early 1970s when such products came into wide use. Population-based surveys in the U.S. Southwest (Franco et al., 1985) and in Minnesota (Folsom et al., 1983) indicate that 85 to 90% of high blood pressure cases are now detected and under therapeutic control in urban areas. Estimating the proportion of cases of hypertension in the population attributed to a known risk factor (the population-attributable fraction) indicates the potential impact that effective reduction in the risk factor could have in reducing hypertension-associated mortality in the population. Calculation of the attributable fraction for all known risk related to hypertension suggests that effective control of hypertension in the population could result in a 20% reduction in all-cause mortality among whites along with a 30% reduction among black men and a 45% reduction among black women based on mortality rates among nonhypertensives. The estimated decline in death rates is similar to the observed decline in the age-adjusted U.S. mortality from 1968 to 1975. It is therefore likely that part of the decline in cardiovascular deaths as well as in all-cause deaths since 1972 is attributable to the improved medical control of hypertension. However, the actual contribution of control may be less than this estimation (Bonita and Beaglehole, 1986). Associations Between Risk Factors in Individuals and Hypertension Age As shown in Figure 5-3, systolic blood pressure rises steeply from infancy to adulthood (Voors et al., 1978) and levels off once adult height is reached. The age-related upward trend in mean systolic pressure occurs across most adult populations. Cross-sectional and cohort data from the Framingham Study (Kannel, 1980) give a somewhat different picture of therelationship of systolic and diastolic blood pressure to age in adults (Figure FIGURE 5-3 Changes in mean systolic blood pressures from infancy to age 70 in nine studies Comstock, 1957; Hamilton et al., 1954; Johnson et al., 1965; Miall and Lovell, 1967; Nance et al., 1965; Roberts and Maurer, 1976; Robinson and Brucer, 1939; Stocks, 1954. From Voors et al. (1978).
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Page 126 the ninth leading cause of death for all ages, accounting for 28,000 deaths (NIAAA, 1985). In other countries, marked fluctuations in mortality from alcoholic cirrhosis have accompanied drastic changes in the availability of beverage alcohol. The most dramatic example occurred in France, where the rates fell from approximately 35 per 100,000 before World War II to about 6 per 100,000 during the war, and then increased to 35 or more per 100,000 after the war (Terris, 1967). Less dramatic but similar changes over time have been observed in other countries. Associations Between Risk Factors in Individuals and Alcoholic Cirrhosis Alcoholic cirrhosis has consistently been correlated predominantly with the per-capita consumption of alcohol on a national basis (Gordis et al., 1983). In turn, alcohol consumption and alcoholic cirrhosis have been correlated positively with the availability and the ease of access to alcohol as stated above, and inversely with cost (Terris, 1967). Rates of mortality from alcoholic cirrhosis are twofold higher in males than in females, are negligible under 25 years of age, are appreciable in the 25- to 44-year age group (8.6/10,000), peak from age 45 to 64 (39.2/100,000), and decline slightly after age 65 (36.7/100,000) (DHEW, 1979b). The risk of alcoholic cirrhosis from lifetime alcohol consumption was expressed in a mathematical model by Skog (1984). Most alcoholics develop cirrhosis only after many years of alcohol abuse, and the risk increases as a function of any suitable measure of consumption. More than 50% of the risk is determined by current intake plus the preceding 5 years of consumption. Consumption rates during the preceding 6 to 25 years contribute to the balance of the risk, but the weight of the predictive power for each of those years is much less. This model of risk is consistent with observations that mortality due to most chronic progressive diseases decreases rapidly when the causative agent is removed. Gallbladder Disease and Gallstones Population Differences in Frequency Among Countries The prevalence of gallstones also varies widely among countries, but reliable data are difficult to obtain because gallstones are difficult to detect in population surveys. Furthermore, although they are frequent causes of morbidity, they do not often cause death. Thus, mortality rates cannot be used as indices of occurrence. The prevalence of gallstones at autopsy is high (affecting 10% or more of all adults) in the industrialized countriesin the United States, Australia, and Europe. It is lower (5% or less) in the nonindustrialized countries of Asia and Africa (Brett and Barker, 1976). However, there have been no systematic population surveys using similar methods in different areas to compare gallstone prevalence among countries or morbidity related to gallstones. Within Countries In most countries, the prevalence of gallstones is two to three times higher in women than in men (Brett and Barker, 1976). In the United States, Native Americans and people descended from an admixture of New World natives (such as Latin Americans or Mexican Americans) have a much higher prevalence of gallstones than those with a West European heritage (Arevalo et al., 1987; Comess et al., 1967; Hesse, 1959; Sampliner et al., 1970; Weiss et al., 1984). Three-fourths of middle-aged Pima Indian women had evidence of gallbladder disease when surveyed by cholecystography, and approximately 80% of those with abnormal cholecystograms were found to have gallstones at surgery or at autopsy (Sampliner et al., 1970). Thus, the prevalence of gallstones in adult Pima women exceeds 50%, compared to estimates of 10 to 20% for comparable U.S. whites and blacks. In Migrants Information comparing the frequency of gallstones and gallbladder disease in migrants with that in their countries of origin is limited. Data do suggest, however, that environmental factors (e.g., diet) may influence risk. A survey of hospital admissions in Hawaii showed that Chinese had the highest admission rate for gallbladder disease. In contrast, gallbladder disease is reported to be rare among native Chinese living in China (Yamase and McNamara, 1972). Time Trends in Mortality and Morbidity There is no information regarding changes in prevalence of gallstones or gallbladder disease over time in the United States. In Japan, evidence suggests that the prevalence of gallstones at autopsy increased about threefold between 1950 and 1970 (Nagase et al., 1978).
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Page 127 Associations Between Risk Factors in Individuals and Gallbladder Disease and Gallstones Being a female and being obese are most consistently associated with gallstones (reviewed by Bennion and Grundy, 1978a,b, and by Low-Beer, 1985). Obesity is also related to supersaturation of gallbladder bile, and gallstones have been linked with high-calorie diets, but not with cholesterol intake, type of dietary fat, or dietary fiber (Bennion and Grundy, 1978a,b). In an analysis of the Framingham cohort after 10 years of observation, incidence of gallbladder disease (principally cholelithiasis) was twice as high in women as in men and was associated with an increase in weight and number of pregnancies, but was not related to serum cholesterol concentration, cigarette smoking, physical activity, CHD, or intakes of alcohol, cholesterol, fat, or protein (Friedman et al., 1966). In Japan, a review of surgical patients indicated that younger people had more cholesterol-containing gallstones (Nagase et al., 1978). Dental Caries Dental caries is localized demineralization of the tooth surface caused primarily by organic acid metabolites of oral microorganisms. The disease leads to a chronic progressive destruction of the teeth. In epidemiologic studies, caries prevalence is expressed as decayed, missing, and filled teeth (dmft) for primary dentition and as DMFT for permanent teeth. Population Differences in Prevalence Among Countries Sreenby (1982) compared the prevalence of dental caries in children ages 6 (in 23 countries) and 12 (in 47 countries) using data obtained from the World Health Organization's Global Oral Epidemiology Bank (Barmes and Sardo-Infirri, 1977). The dmft and DMFT values used by Sreenby (1982) are indices of the cumulative effect of dental caries over the life of the dentition. Thus, for the primary dentition in 6-year-olds, the exposure period was approximately 4 to 5 years; for permanent teeth in the 12-year-olds, the period was 4 to 6 years for the molars and anterior teeth. Prevalence of DMFT in the 6-year-olds surveyed ranged from 0.9 per child in Cameroon to 9.3 in Japan. Prevalence was highest in Asian countries and lowest in the African countries surveyed except in South Africa, which had an intermediate level (4.4) similar to that of the United States (3.4) and the United Kingdom (4.5). The prevalence of DMFT among 12-year-old children ranged from 0.1 in Zambia to 10.6 in Switzerland. Again, the mean DMFT tended to be lowest in African countries; however, unlike the prevalence for 6-year-olds, the DMFT prevalence for 12-year-olds was highest in Switzerland and in the northern European countries of Denmark and Finland. Rates for Asian countries tended to be intermediate like those of the United States (4.0) and the United Kingdom (5.5) Within Countries Striking differences in the prevalence of caries in the U.S. population by geographic area were noted in the 1980 national survey of caries in schoolchildren (NIDR, 1981). Caries prevalence was highest in the Northeast, lowest in the Southwest, and at intermediate levels elsewhere. According to data derived from the the National Health Survey for 1971 to 1973 (NIDR, 1981), people of both sexes and all ages (1 to 74 years) had an average of 13 decayed, missing, and filled permanent teeth. A closer review of this figure indicates that there was an average of 1.3, 5.3, and 6.4 decayed, missing, and filled teeth, respectively. An estimated 14.7% of the adults (18 to 74 years old) had lost all their permanent teeth. In a study of the oral health of U.S. adults, completed in 1986, only 4% of people of ages 18 to 65 were edentulous (Miller et al., 1987). In Migrants No information on caries in migrants was found. Time Trends Until the 1970s, caries was most prevalent (affecting 95% of the population) in developed countries, especially in those with diets high in refined carbohydrates. The only exception occurred during and just after World War II, when the prevalence rates of caries dropped precipitously, although temporarily, in children living in Europe (Sognnaes, 1948; Toverud, 1957) and Japan (Takeuchi, 1961). During the 1970s, the prevalence of caries declined dramatically again among school-aged children not only in many countries of western Europe but also in North America (Glass, 1982). In contrast, the rate of caries is increasing in many Third World countries (Barmes and Sardo-Infirri, 1977).
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Page 128 In the 1971-1973 National Health Survey, children between the ages of 5 and 17 had decay or fillings in an average of 7.06 teeth (NIDR, 1981). By 1981, this number had dropped to 4.77 (NIDR, 1981). Likewise, as noted above, the prevalence of edentulia dropped from 14.7% in 18- to 74-year-old people during 1971-1973 (NIDR, 1981) to 4% in the 18- to 65-year age group in 1986 (Miller et al., 1987). There are reports that root surface caries is becoming more prevalent among older peoplea result perhaps of decreased edentulia (Seichter, 1987). This is discussed in the next section. Associations Between Risk Factors in Individuals and Dental Caries Age Caries of the tooth crown is predominantly a disease of children and adolescents. It begins as soon as teeth erupt; incidence remains high, and prevalence increases linearly up to ages 18 to 20. After age 25 or so, the incidence of coronal caries diminishes, but the disease may still occur. The epidemiologic study of caries in adults becomes increasingly complicated by the fact that it is often not possible to distinguish between teeth lost because of caries and those missing because of periodontal and other oral diseases. What is certain is that caries of the root surface of the teeth, secondary to exposure of the root by recession of the gingivae, becomes increasingly prevalent with advancing age. In a national survey of employed U.S. adults, completed in 1986 (Miller et al., 1987), root-surface caries had affected approximately 60% of the population by age 65; the average was about three lesions per person. Sex Caries prevalence is higher among females than among males at every age. This observation is only partly explained by the earlier eruption of teeth in females, leading to longer exposure to the oral environment. Root-surface caries is more common in males for reasons that are not yet clear (Carlos, 1984). Racial, Ethnic, and Socioeconomic Differences Chung et al. (1970) analyzed the relationship of race to caries prevalence in 9,912 12- to 18-year-old children in Hawaii. They noted that dental caries was most prevalent among children of Japanese origin, followed by children of Hawaiian origin. Children with Caucasian, Puerto Rican, or Filipino parentage had the lowest caries activity. In a subsequent survey of 910 eighth-grade students in Hawaii, Hankin et al. (1973) found that the prevalence of caries in Hawaiian children had surpassed that in children of Japanese ancestry. Caucasian children continued to enjoy the lower rates. A 1980 U.S. national survey (NIDR, 1981) showed no notable differences in caries prevalence with respect to color, ethnic group, or socioeconomic status. However, the HHANES (Hispanic Health and Nutrition Examination Survey) of 1982-1984 indicated that Mexican-American children residing in the Southwest had a dental caries distribution similar to that of other groups in the region, but that Mexican-American children from low-income families had nearly two times more decayed teeth than did Mexican-American children from high income families (Ismail et al., 1987). Occupational and Psychosocial Risk Factors No information on caries was found in these areas. Familial and Genetic Factors There is some evidence of genetic predisposition to caries (Witkop, 1962), but this appears to be a minor etiologic factor compared to the local influences of diet, bacterial deposits on teeth, and less than optimal ingestion of fluoride. References Abbott, R.D., Y. Yin, D.M. Reed, and K. Yano. 1986. Risk of stroke in male cigarette smokers. N. Engl. J. Med. 315: 717-720. Abraham, S., M.D. Carroll, M.F. Najjar, and R. Fulwood. 1983. Obese and overweight adults in the United States. Vital and Health Statistics, Series 11, No. 230. DHHS Publ. No. (PHS) 83-1680. National Center for Health Statistics. Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 93 pp. AHA (American Heart Association). 1973. Coronary Risk Handbook: Estimating Risk of Coronary Heart Disease in Daily Practice. American Heart Association, New York. 35 pp. AHA (American Heart Association). 1983. 1984 Heart Facts. Office of Communications, Dallas. 25 pp. Allen, E.V., N.W. Barker, and E.A. Hines, Jr. 1946. Peripheral Vascular Diseases. W.B. Saunders, Philadelphia. 871 pp. Anastasiou-Nana, M., S. Nanas, J. Stamler, J. Marquardt, R. Stamler, H.A. Lindberg, D.M. Berkson, K. Liu, E. Stevens, M. Mansour, and T. Tokich. 1982. Changes in rates of sudden CHD death with first vs. recurrent events,
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Page 129 Chicago Peoples Gas Co. Study, 1960-1980. Circulation, Suppl. 66:11-236. Anthony, P.P., K.G. Ishak, N.C. Nayak, H.E. Poulsen, P.J. Scheuer, and L.H. Sobin. 1977. The morphology of cirrhosis: definition, nomenclature, and classification. Bull. W.H.O. 55:521-540. Arevalo, J.A., A.O. Wollitzer, M.B. Corporon, M. Larios, D. Huante, and M.T. Ortiz. 1987. Ethnic variability in cholelithiasis: an autopsy study. West. J. Med. 147:44-47. Austin, D.F., and K.M. Roe. 1982. The decreasing incidence of endometrial cancer: public health implications. Am. J. Public Health 72:65-68. Barnes, D.E., and J. Sardo-Infirri. 1977. World Health Organization activities in oral epidemiology. Community Dent. Oral Epidemiol. 5:22-29. Beaglehole, R., C.E. Salmond, A. Hooper, J. Huntsman, J.M. Stanhope, J.C. Cassel, and I.A. Prior. 1977. Blood pressure and social interaction in Tokelauan migrants in New Zealand. J. Chronic Dis. 30:803-812. Bennion, L.J., and S.M. Grundy. 1978a. 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Iliushina, and L.S. Gurevich. 1976. Prevalence of ischaemic heart disease, arterial hypertension and intermittent claudication, and distribution of risk factors among middle-aged men in Moscow and Berlin. Cor Vasa 18:104-118. Bouchard, E., L Perusse, C.. Leblanc, A. Tremblay, and G. Theriault. 1988. Inheritance of the amount and distribution of human body fat. Int. J. Obesity 12:205-215. Bray, G.A., ed. 1979. Obesity in America. NIH Publ. No. 79-359. National Institutes of Health, Public Health Service, U.S. Department of Health, Education, and Welfare, Bethesda, Md. 285 pp. Bray, G.A. 1985. Obesity: definition, diagnosis and disadvantages. Med. J. Aust. 142:S2-S8. Bray, G.A. 1987. Obesity and the heart. Modern Concepts Cardiovasc. Dis. 56:67-71. Brett, M., and D.J. Barker. 1976. The world distribution of gallstones. Int. J. Epidemiol. 5:335-341. Brown, J., G.J. Bourke, G.F. Gearty, A. Finnegan, M. Hill, F.C. Heffernan-Fox, D.E. Fitzgerald, J. Kennedy, R.W. Childers, W.J.E. Jessop, M.F. Trulson, M.C. Latham, S. Cronin, M.B. McCann, R.E. Clancy, I. Gore, H.W. Stroudt, D.M. Hegsted, and F.J. Stare. 1970. Nutritional and epidemiologic factors related to heart disease. World Rev. Nutr. Diet. 12:1-42. Carlos, J.P. 1984. Epidemiologic trends in caries: impact on adults and the aged. Pp. 131-148 in B. Guggenheim, ed. Cariology Today. S. Karger, Basel. Carroll, M.D., S. Abraham, and C.M. Dresser. 1983. Dietary Intake Source Data: United States, 1976-1980. Vital and Health Statistics, Series 11, No. 231. DHHS Publ. No. (PHS) 83-1681. National Center for Health Statistics, Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 483 pp. Chung, C.S., D.W. Runck, J.D. Niswander, S.E. Bilben, and M.C.W. Kau. 1970. Genetic and epidemiologic studies of oral characteristics in Hawaii's schoolchildren. I. Caries and periodontal disease. J. Dent. Res. 49:1374-1385. Cohen, A.M., J. Fidel, B. Cohen, A. Furst, and S. Eisenberg. 1979. 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The prevalence of peripheral arterial disease in a defined population. Circulation 71:510-515. Cummings, S.R., J.L. Kelsey, M.C. Nevitt, and K.J. O'Dowd. 1985. Epidemiology of osteoporosis and osteoporotic fractures. Epidemiol. Rev. 7:178-208. Dawber, T.R., and W.B. Kannel. 1972. Current status of coronary prevention. Lessons from the Framingham Study. Prev. Med. 1:499-512. Day, N.E., and N. Munoz. 1982. Esophagus. Pp. 596-623 in D. Schottenfeld and J.F. Fraumeni, Jr., eds. Cancer Epidemi-
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Representative terms from entire chapter: