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Vital exhaustion, defined as a combination of fatigue, lack of energy, feelings of hopelessness, loss of libido, and increased irritability, has been proposed as a risk indicator for the development of coronary heart disease (CHD). It is unclear if the association between vital exhaustion and CHD is independent of sleep behavior, depression, and physical activity. We ascertained sense of exhaustion among 5,053 male college alumni who were free of cardiovascular disease, cancer, and chronic obstructive pulmonary disease by asking, "How often do you experience sense of exhaustion (except after exercise)?" on a health survey in 1980. Eight hundred fifteen men died during 12 years of follow-up, 25% due to CHD. After adjustment for age, body mass index, smoking status, and history of physician-diagnosed diabetes and hypertension, frequent sense of exhaustion was associated with a twofold increase in CHD mortality (rate ratio 2.07; 95% confidence interval 1.08 to 3.96). After additional adjustment for insomnia, sleep duration, use of sleeping pills and tranquilizers, physical activity, history of physician-diagnosed depression, and alcohol intake, the rate ratio was not appreciably altered; however, the association now was of borderline significance (rate ratio 2.06; 95% confidence interval: 0.98 to 4.36) because there were only 10 deaths from CHD among men who were frequently exhausted. In a prospective observational study, frequent sense of exhaustion appeared to be independently associated with increased risk of CHD mortality in men. [ABSTRACT FROM AUTHOR]

Over the past 50 years or so, many epidemiologic studies have examined the association between physical activity or physical fitness and coronary heart disease (CHD) risk. Their findings have been consistent, showing that physically active or fit men and women experience lower CHD risk than those who are sedentary or unfit. On average, active patients have half the risk of sedentary patients. Data regarding the optimal amount, intensity, and duration of physical activity required to decrease CHD risk have been less clear. It appears that following recent recommendations (at least 30 minutes of moderate-intensity physical activity such as brisk walking on most days) is sufficient.

Background: Physical activity is associated with a decreased risk of coronary heart disease (CHD). However, it is unclear whether the duration of exercise episodes is important: Are accumulated shorter sessions as predictive of decreased risk as longer sessions if the same amount of energy is expended?, Methods and Results: In the Harvard Alumni Health Study, we prospectively followed 7307 Harvard University alumni (mean age 66.1 years) from 1988 through 1993. At baseline, men reported their walking, stair climbing, and participation in sports or recreational activities. For each of the latter activities, they also reported the frequency and average duration per episode. During follow-up, 482 men developed CHD. In age-adjusted analysis, a longer duration of exercise episodes predicted lower CHD risk (P: trend=0.04). However, after total energy expended on physical activity and potential confounders was accounted for, duration no longer had an independent effect on CHD risk (P: trend=0.25); that is, longer sessions of exercise did not have a different effect on risk compared with shorter sessions, as long as the total energy expended was similar. In contrast, higher levels of total energy expenditure significantly predicted decreased CHD risk in both age-adjusted (P: trend=0.009) and multivariate (P: trend=0.046) analyses., Conclusions: These data clearly indicate that physical activity is associated with decreased CHD risk. Furthermore, they lend some support to recent recommendations that allow for the accumulation of shorter sessions of physical activity, as opposed to requiring 1 longer, continuous session of exercise. This may provide some impetus for those sedentary to become more active.

The evidence for a protective effect of vegetables, fruits, and legumes against prostate cancer is weak and inconsistent. We examined the relationship of these food groups and their constituent foods to prostate cancer risk in a multicenter case-control study of African-American, white, Japanese, and Chinese men. Cases (n = 1619) with histologically confirmed prostate cancer were identified through the population-based tumor registries of Hawaii, San Francisco, and Los Angeles in the United States and British Columbia and Ontario in Canada. Controls (n = 1618) were frequency-matched to cases on ethnicity, age, and region of residence of the case, in a ratio of approximately 1:1. Dietary and other information was collected by in-person home interview; a blood sample was obtained from control subjects for prostate-specific antigen determination. Odds ratios (OR) were estimated using logistic regression, adjusting for age, geographic location, education, calories, and when indicated, ethnicity. Intake of legumes (whether total legumes, soyfoods specifically, or other legumes) was inversely related to prostate cancer (OR for highest relative to lowest quintile for total legumes = 0.62; P for trend = 0.0002); results were similar when restricted to prostate-specific antigen-normal controls or to advanced cases. Intakes of yellow-orange and cruciferous vegetables were also inversely related to prostate cancer, especially for advanced cases, among whom the highest quintile OR for yellow-orange vegetables = 0.67 (P for trend = 0.01) and the highest quintile OR for cruciferous vegetables = 0.61 (P for trend = 0.006). Intake of tomatoes and of fruits was not related to risk. Findings were generally consistent across ethnic groups. These results suggest that legumes (not limited to soy products) and certain categories of vegetables may protect against prostate cancer.

Context: Recent guidelines for treatment of overweight and obesity include recommendations for risk stratification by disease conditions and cardiovascular disease (CVD) risk factors, but the role of physical inactivity is not prominent in these recommendations., Objective: To quantify the influence of low cardiorespiratory fitness, an objective marker of physical inactivity, on CVD and all-cause mortality in normal-weight, overweight, and obese men and compare low fitness with other mortality predictors., Design: Prospective observational data from the Aerobics Center Longitudinal Study., Setting: Preventive medicine clinic in Dallas, Tex., Participants: A total of 25714 adult men (average age, 43.8 years [SD, 10.1 years]) who received a medical examination during 1970 to 1993, with mortality follow-up to December 31, 1994., Main Outcome Measures: Cardiovascular disease and all-cause mortality based on mortality predictors (baseline CVD, type 2 diabetes mellitus, high serum cholesterol level, hypertension, current cigarette smoking, and low cardiorespiratory fitness) stratified by body mass index., Results: During the study period, there were 1025 deaths (439 due to CVD) during 258781 man-years of follow-up. Overweight and obese men with baseline CVD or CVD risk factors were at higher risk for all-cause and CVD mortality compared with normal-weight men without these predictors. Using normal-weight men without CVD as the referent, the strongest predictor of CVD death in obese men was baseline CVD (age- and examination year-adjusted relative risk [RR], 14.0; 95% confidence interval [CI], 9.4-20.8); RRs for obese men with diabetes mellitus, high cholesterol, hypertension, smoking, and low fitness were similar and ranged from 4.4 (95% CI, 2.7-7.1) for smoking to 5.0 (95% CI, 3.6-7.0) for low fitness. Relative risks for all-cause mortality in obese men ranged from 2.3 (95% CI, 1.7-2.9) for men with hypertension to 4.7 (95% CI, 3.6-6.1) for those with CVD at baseline. Relative risk for all-cause mortality in obese men with low fitness was 3.1 (95% CI, 2.5-3.8) and in obese men with diabetes mellitus 3.1 (95% CI, 2.3-4.2) and as slightly higher than the RRs for obese men who smoked or had high cholesterol levels. Low fitness was an independent predictor of mortality in all body mass index groups after adjustment for other mortality predictors. Approximately 50% (n = 1674) of obese men had low fitness, which led to a population-attributable risk of 39% for CVD mortality and 44% for all-cause mortality. Baseline CVD had population attributable risks of 51% and 27% for CVD and all-cause mortality, respectively., Conclusions: In this analysis, low cardiorespiratory fitness was a strong and independent predictor of CVD and all-cause mortality and of comparable importance with that of diabetes mellitus and other CVD risk factors.

Purpose: This investigation quantifies the relation between cardiorespiratory fitness levels and cardiovascular disease (CVD) mortality within strata of other CVD predictors., Methods: Participants included 25,341 male Cooper Clinic patients who underwent a maximal graded exercise test. CVD death rates were determined for low (least fit one-fifth), moderate (next two-fifths), and high (top two-fifths) cardiorespiratory fitness categories by strata of smoking habit, blood cholesterol level, resting blood pressure, and health status. There were 226 cardiovascular deaths during 211,996 man-years of follow-up., Results: For individuals with none of the major CVD predictors (smoking, elevated resting systolic blood pressure, elevated blood cholesterol), there was a strong inverse relation (P = 0.001) between fitness level and CVD mortality. An inverse relation between CVD mortality and fitness level was seen within strata of cholesterol levels and health status. No evidence of a trend (P = 0.60) for decreased mortality was seen across fitness levels for individuals with elevated systolic blood pressure; however, a strong inverse gradient (P < 0.001) was seen across fitness levels for individuals with normal systolic blood pressure. There was a tendency for association between high levels of fitness and decreased CVD mortality in smokers compared with low and moderately fit smokers (P < 0.076). There was no significant association between level of fitness and CVD mortality for individuals with multiple (two or more) predictors (P = 0.325). Approximately 20% of the 226 CVD deaths in the population studied were attributed to low fitness level., Conclusions: Moderate and high levels of cardiorespiratory fitness seem to provide some protection from CVD mortality, even in the presence of well established CVD predictors.

Longitudinal observations on the sports play, social habits and health status of 52,000 men who entered Harvard College or the University of Pennsylvania between 1916 and 1950 have afforded means of identifying causes of disease and death. These observations were then translated into the eff ect of sports and physical exercise on health and longevity. Student sports play in college predicted a decreased risk of developing cardiovascular disease (CVD) at least up to age 50 years. Questionnaire surveys showed physical exercise (sports play, walking and stair climbing) in middle age to be inversely related to the later development of CVD and early death. In a 10-year follow-up between 1962 and 1972, alumni aged 35-74 years who expended greater than or equal to ≥ 2000 kcal week(-1) (8.4 MJ week -1 ) in such activities had a 25% reduced risk of CVD and death compared with less active men. But, the 'protective eff ect' of early athleticism waned unless a physically active life was maintained. In contrast, sedentary students who took up an active life were at a lower risk of CVD and death than former student athletes who gave up or reduced their physical activities in middle age. A total of 17,815 Harvard alumni aged 45-84 years were followed from a 1977 questionnaire survey through 1992, with 4399 deaths occurring. Death rates declined with increased levels of total activity (estimated in kilocalories), and declined also with increased intensity of effort measured as from none, to light, to moderately vigorous or vigorous sports play. Death rates at any given quantity of physical exercise were lower for men playing moderately intense sports than for less vigorous men. Over the age range, in the 16-year follow-up, Harvard alumni playing moderately vigorous or more intense sports gained 1.5 years by age 90 compared with less active men.

Background: Fourfold to sixfold higher prostate cancer rates in Japanese-American men in the United States compared with Japanese men in Japan have been cited to support a role for environmental risk factors in the etiology of the disease. To examine the hypothesis that part or all of the elevated prostate cancer rates in Japanese-American men may reflect more intensive prostate cancer screening in the United States than in Japan, we compared prostate-specific antigen (PSA) levels in community-based samples of serum from men without prostate cancer., Methods: Japanese-American men aged 40-85 years and native Japanese men aged 40-89 years with no history of prostate cancer provided sera, respectively, in the United States from March 1990 through March 1992 (n = 237) or in Japan from January 1992 through December 1993 (n = 3522). Age-specific PSA levels were used to estimate the prevalences of undetected prostate cancer in the two populations., Results: Age-specific mean PSA levels were significantly lower in Japanese-Americans than in native Japanese (two-sided P<.001). The prevalence of an elevated PSA level increased with age in both populations and exceeded 5% among men aged 60 years or more. Combined with data on prevalence of detected prostate cancer in the two populations, our data suggest that some 10.0% of Japanese-Americans aged 75 years have prostate cancer, with 31% of that fraction remaining undiagnosed. The corresponding estimates in Japan are a total cancer prevalence of 5.4%, of which 81% has not been detected clinically., Conclusions: The total cancer prevalence ratio 10.0/5.4 = 1.9 (95% confidence interval = 1.5-2.3) in Japanese-American men compared with Japanese men in Japan suggests an increased risk for Japanese-American men, but of less magnitude than the fourfold to sixfold increase indicated by the incidence data.

Objective: To quantify the relation of cardiorespiratory fitness to cardiovascular disease (CVD) mortality and to all-cause mortality within strata of other personal characteristics that predispose to early mortality. DESIGN--Observational cohort study. We calculated CVD and all-cause death rates for low (least fit 20%), moderate (next 40%), and high (most fit 40%) fitness categories by strata of smoking habit, cholesterol level, blood pressure, and health status., Setting: Preventive medicine clinic., Study Participants: Participants were 25341 men and 7080 women who completed preventive medical examinations, including a maximal exercise test., Main Outcome Measures: Cardiovascular disease and all-cause mortality., Results: There were 601 deaths during 211996 man-years of follow-up, and 89 deaths during 52982 woman-years of follow-up. Independent predictors of mortality among men, with adjusted relative risks (RRs) and 95% confidence intervals (CIs), were low fitness (RR, 1.52;95% CI, 1.28-1.82), smoking (RR, 1.65; 95% CI, 1.39-1.97), abnormal electrocardiogram (RR, 1.64;95% CI, 1.34-2.01), chronic illness (RR, 1.63;95% CI, 1.37-1.95), increased cholesterol level (RR, 1.34; 95% CI, 1.13-1.59), and elevated systolic blood pressure (RR, 1.34; 95% CI, 1.13-1.59). The only statistically significant independent predictors of mortality in women were low fitness (RR, 2.10; 95% Cl, 1.36-3.21) and smoking (RR, 1.99; 95% Cl, 1.25-3.17). Inverse gradients were seen for mortality across fitness categories within strata of other mortality predictors for both sexes. Fit persons with any combination of smoking, elevated blood pressure, or elevated cholesterol level had lower adjusted death rates than low-fit persons with none of these characteristics., Conclusions: Low fitness is an important precursor of mortality. The protective effect of fitness held for smokers and nonsmokers, those with and without elevated cholesterol levels or elevated blood pressure, and unhealthy and healthy persons. Moderate fitness seems to protect against the influence of these other predictors on mortality. Physicians should encourage sedentary patients to become physically active and thereby reduce the risk of premature mortality.

Differences in endogenous androgen levels have been hypothesized to explain ethnic differences in prostate cancer risk. To examine this hypothesis, we gathered data on serum concentrations of androgens and sex hormone-binding globulin (SHBG) in healthy older men from four ethnic groups at different levels of prostate cancer risk. As part of a population-based case-control study of prostate cancer we conducted in California, Hawaii, and Vancouver, Canada, 1127 African-American, white, Chinese-American, and Japanese-American control men, mostly ages 60 years or older (mean age, 69.9 years) provided information on various lifestyle factors and donated an early morning fasting blood sample between March 1990 and March 1992. We used these data to examine the distributions of serum androgens [testosterone (total, free, and bioavailable), dihydrotestosterone (DHT)], the ratio of DHT to total testosterone (DHT:testosterone ratio), and SHBG in these four ethnic groups. We also assessed correlations between concentrations of these measures with age, body size, physical activity, and other personal characteristics, and we evaluated ethnic differences in concentrations of androgens and SHBG after adjusting for these characteristics. In each of the four ethnic groups, concentrations of free and bioavailable testosterone declined with age, whereas SHBG concentrations increased with age. Age-adjusted concentrations of all androgen measures and SHBG decreased with increasing levels of Quetelet's index. After adjustment for age and Quetelet's index, androgens and SHBG showed no clear and consistent relationships to physical activity, alcohol consumption, or tobacco use. DHT:testosterone ratio was higher in men reporting a history of benign prostate disease than in men without such a history, and higher in vasectomized men than in nonvasectomized men. SHBG concentrations were higher in men reporting one or more first-degree relatives with prostate cancer than in men without such a family history. After adjustment for age and Quetelet's index, the levels of total and bioavailable testosterone were highest in Asian-Americans, intermediate in African-Americans, and lowest in whites. However, the DHT:testosterone ratio was highest in African-Americans, intermediate in whites, and lowest in Asian-Americans, corresponding to the respective incidence rates in these groups and providing indirect evidence for ethnic differences in 5alpha-reductase enzyme activity.

We studied the adoption or maintenance of physical activity and other optional lifeway patterns for their influence on mortality rates of Harvard College alumni. Men aged 45-84 in 1977, surveyed by questionnaire in 1962 or 1966 and again in 1977, were followed from 1977 through 1988 or to age 90. Of 14,786 alumni, 2,343 died in 165,402 man-years of follow-up. Relative risks of death, standardized for potential confounding influences, for men who between questionnaires increased their physical activity through walking, stair climbing, and sports or recreational activities to 1,500 kcal or more per wk were 0.72 (95% confidence interval 0.64-0.82), compared with 1.00 for men who remained less active. Corresponding relative risks for men who adopted moderately vigorous sports play (> or = 4.5 METs) were 0.73 (0.65-0.81) vs 1.00 for men not adopting such sports; and for cigarette smokers who quit, 0.74 (0.65-0.84) vs 1.00 for persistent smokers. Men with recently diagnosed hypertension had a lower death risk than long-term hypertensives (0.80; 0.70-0.92), as did men with consistent normotension (0.52; 0.47-0.58). Changes in body-mass index had little influence on mortality during follow-up. These findings fit the hypothesis that adopting a physically active lifeway, quitting cigarette smoking, and remaining normotensive independently delay all-cause mortality and extend longevity.

Physical activity has been recommended by physicians in managing patients with noninsulin-dependent diabetes mellitus (NIDDM); however, it is unclear whether physical activity can prevent this disease. Several prospective studies have suggested that increased physical activity may lead to the prevention of NIDDM. In the University of Pennsylvania Alumni Health Study, 5990 men were surveyed to determine the relationship between physical activity and the development of NIDDM. A total of 202 men developed NIDDM from 1962 to 1976. Leisure-time physical activity, expressed in kilocalories (kcal) was inversely related to the development of NIDDM. Incidence rates declined as energy expenditure increased. For each 2000-kcal increment in energy expenditure, the risk of NIDDM was reduced by 24% [relative risk (RR) 0.76, 95% confidence interval (CI) 0.63-0.92]. This association remained when adjusting for obesity, hypertension, and parental history of diabetes. The protective effect of physical activity was strongest in individuals at highest risk for NIDDM. Based on the review of data from several large prospective studies, it is quite likely that increased levels of physical activity are effective in preventing NIDDM, and the protective benefit is especially pronounced in those individuals who have the highest risk of disease.

Previous investigations regarding the influence of physical activity on cancer risk generally have utilized a single assessment of activity, thus failing to account for changes over time. Additionally, one assessment may be somewhat imprecise. We attempted to overcome these problems in a study of 17,607 men (aged 30-79 yr), followed from 1962 or 1966 (1962/1966) through 1988. We assessed physical activity (based on self-reported stair climbing, walking and participation in sports or recreational activities) twice: in 1962/1966 and again in 1977. A total of 280 colon, 53 rectal, 454 prostatic, 262 lung, and 88 pancreatic cancers developed during follow-up. Among alumni with Quetelet's index > or = 26 units, those highly active (energy expenditure > or = 2,500 kcal [> or = 10,460 kJ].wk-1) had 0.19 (95% confidence interval, 0.02-1.52) to 0.56 (0.29-1.09) times the colon cancer risk of those inactive (< 1,000 kcal [< 4,184 kJ].wk-1). Colon cancer risk was unrelated to level of activity among alumni with Quetelet's index < 26 units. Highly active alumni also had 0.39 (95% confidence interval, 0.18-0.85) to 0.62 (0.45-0.85) times the lung cancer risks of their inactive colleagues. Physical activity was not significantly associated with risks of rectal, prostatic, or pancreatic cancers. The biologic basis for a protective effect of increased activity on cancer risk appears plausible.

The validity and reproducibility of the Physical Activity Index from the College Alumnus Questionnaire (PAI-CAQ) were determined in 78 men and women (21-59 yr) with a broad range of physical activity habits. The PAI-CAQ was computed as the sum of energy expended in stair climbing, walking, and sports and recreational physical activity recalled from the past week. Data were validated against measures of cardiorespiratory fitness, body fatness, motion detection, and physical activity records. All physical activity was recorded by participants for six 48-hour periods. Each day of the week, including weekends, were represented at least twice in the physical activity records. Age-adjusted correlation coefficients between like activities on the College Alumnus Questionnaire and physical activity records ranged from 0.25 to 0.65 in men and 0.28 to 0.86 in women. Correlations between the PAI-CAQ and validation criteria that reflected total and heavy-intensity physical activities were higher (r = 0.34-0.69, p < 0.05) than for lighter-intensity physical activities and motion detection expressed in MET-min.d-1 and kcal.d-1 (r < 0.35, p > 0.05). Test-retest reproducibility was higher over 1 month (r = 0.72) than over 8 and 9 months (r = 0.34 and 0.43) (p < 0.05). Energy expended in walking and stair climbing was underestimated on the College Alumnus Questionnaire, resulting in lower PAI-CAQ scores, as compared to the physical activity records.

Background: Recent trends toward increasing physical exercise, stopping cigarette smoking, and avoiding obesity may increase longevity. We analyzed changes in the lifestyles of Harvard College alumni and the associations of these changes with mortality., Methods: Men who were 45 to 84 years of age in 1977 and who had reported no life-threatening disease on questionnaires completed in 1962 or 1966 and again in 1977 were classified according to changes in lifestyle characteristics between the first and second questionnaires. We analyzed changes in their level of physical activity, cigarette smoking, blood pressure, and body weight, and the relation of these factors to mortality between 1977 and 1985., Results: Of the 10,269 men, 476 died during this period (which totaled 90,650 man-years of observation). Beginning moderately vigorous sports activity (at an intensity of 4.5 or more metabolic equivalents) was associated with a 23 percent lower risk of death (95 percent confidence interval, 4 to 42 percent; P = 0.015) than not taking up moderately vigorous sports. Quitting cigarette smoking was associated with a 41 percent lower risk (95 percent confidence interval, 20 to 57 percent; P = 0.001) than continuing smoking, but with a 23 percent higher risk than constant nonsmoking. Men with recently diagnosed hypertension had a lower risk of death than those with long-term hypertension (relative risk, 0.75; 95 percent confidence interval, 0.55 to 1.02; P = 0.057), as did men with consistently normal blood pressure (relative risk, 0.52; 95 percent confidence interval, 0.40 to 0.68; P < 0.001). Maintenance of lean body mass was associated with a lower mortality rate than long-term, recent, or previous obesity. The associations between changes in lifestyle and mortality were independent and were largely undiminished by age. Our findings on death from coronary heart disease mirrored those on death from all causes., Conclusions: Beginning moderately vigorous sports activity, quitting cigarette smoking, maintaining normal blood pressure, and avoiding obesity were separately associated with lower rates of death from all causes and from coronary heart disease among middle-aged and older men.

A coding scheme is presented for classifying physical activity by rate of energy expenditure, i.e., by intensity. Energy cost was established by a review of published and unpublished data. This coding scheme employs five digits that classify activity by purpose (i.e., sports, occupation, self-care), the specific type of activity, and its intensity as the ratio of work metabolic rate to resting metabolic rate (METs). Energy expenditure in kilocalories or kilocalories per kilogram body weight can be estimated for all activities, specific activities, or activity types. General use of this coding system would enhance the comparability of results across studies using self reports of physical activity.

For physical activity surveys that would identify relations to chronic diseases, quality of life, and longevity, the method of choice remains the questionnaire, especially if it can be standardized and administered in uniform fashion to large populations. A sample questionnaire derived largely from epidemiological experience with the Harvard Alumni Health Study is presented that requests anthropometric estimates; physician-diagnosed diseases by year of onset; contemporary physical activities including walking, stair-climbing, and recreational pursuits; food-frequency data that estimate nutrient values and caloric intakes; and social habits affecting health. The questionnaire presents opportunities for cross-sectional, retrospective, and prospective studies. Personal characteristics, physical activities, and other elements of lifestyle may be used as predictor or outcome variables in testing specific hypotheses. Representative surveys are described that have validated and used questionnaires of various complexities, some complemented by measures of physiological fitness. The epidemiological survey questionnaire, when properly designed and administered, can measure effectively energy intake, energy retention, energy expenditure, physiological fitness, quality of life, and health maintenance.

Objective: To investigate the effect of body weight change on longevity., Design: Cohort analytic study, following men from 1977 through 1988., Setting: The study was conducted among Harvard University alumni with mean age of 58 years., Patients: Alumni, free of cardiovascular disease and cancer, completed questionnaires on weight, height, cigarette habit, and physical activities in 1962 or 1966 and in 1977 (n = 11,703). We assessed weight change between questionnaires, based on self-reported weights., Main Outcome Measure: Mortality from all causes (n = 1441), coronary heart disease (n = 345), and cancer (n = 459), determined from death certificates., Results: Lowest all-cause mortality was among alumni maintaining stable weight (+/- 1 kg). With this category as referent (relative risk = 1.00), relative risks of death associated with losing more than 5 kg, losing between 1 and 5 kg, (more than 1 kg and up to 5 kg) gaining between 1 and 5 kg (more than 1 kg and up to 5 kg), and gaining more than 5 kg were 1.57 (95% confidence interval, 1.34 to 1.84), 1.26 (1.10 to 1.46), 1.06 (0.90 to 1.24), and 1.36 (1.11 to 1.66), respectively. For coronary heart disease mortality, relative risks were 1.75 (1.26 to 2.43), 1.43 (1.05 to 1.93), 1.28 (0.91 to 1.80), and 2.01 (1.36 to 2.97), respectively. Weight change did not predict cancer mortality. Findings were not explained by cigarette habit, physical activity, or body mass index. We observed similar trends for follow-up between 1977 and 1982 and between 1983 and 1988. Those losing or gaining more weight also reported greater total lifetime weight loss, which may indicate weight cycling., Conclusions: Both body weight loss and weight gain are associated with significantly increased mortality from all causes and from coronary heart disease but not from cancer.

Background: While previous studies suggest that overweight, middle-aged men may face increased risk of colon cancer, it is unclear whether their weights as young adults influence this risk. It is also unknown whether their level of physical activity affects their risk of developing colon cancer., Purpose: To determine the relationship between being overweight in middle-age or young adulthood and colon cancer risk, we prospectively studied alumni of Harvard University. We also investigated whether being overweight influences risk differently for men with different levels of physical activity., Methods: In 1962 or 1966 (1962/1966), alumni completed questionnaires on weight, height, other sociodemographic characteristics, and medical history. We obtained information on weight and height at college entry from university archives. Alumni (n = 17,595) were followed from 1962/1966 to 1988 for colon cancer occurrence, ascertained from follow-up questionnaires in 1977 and 1988 and death certificates., Results: Between 1962/1966 and 1988, 302 cases of colon cancer were diagnosed. Colon cancer risk increased with higher levels of Quetelet's index (weight [kg]/height [m]2) in 1962/1966. Relative risk per unit increase, adjusted for age, physical activity, and parental history of cancer, was 1.08 (95% confidence interval [CI], 1.04-1.13). Quetelet's index at college entry did not predict risk as well (adjusted relative risk per unit increase, 1.05; 95% CI, 1.00-1.10). The heaviest fifth of alumni during both college time and in 1962/1966 had almost two and one-half times the risk of the lightest fifth of alumni (adjusted relative risk, 2.40; 95% CI, 1.40-4.13). When alumni were classified according to activity level in 1962/1966, higher levels of Quetelet's index were significantly associated with colon cancer risk only among those who were less active., Conclusions: Overweight during middle-age or young adulthood is associated with higher colon cancer risk; in overweight, physically active men, however, the risk of colon cancer may not be increased.

The assessment of physical activity at a single time to evaluate its association with cancer may be limited, since such a measure may not adequately reflect activity over the long term. To overcome this limitation, we studied 17,148 Harvard alumni aged 30-79 years who were followed prospectively for the occurrence of colon cancer (n = 225) and rectal cancer (n = 44) from 1965 through 1988. Physical activity, based on self-reported stair climbing, walking, and sports play, was assessed in either 1962 or 1966 (1962/1966) and again in 1977. The increased activity evaluated using either assessment (1962/1966 or 1977) taken alone was not associated with risk of colon cancer. However, alumni who were highly active (energy expenditure of greater than 2500 kilocalories/wk) at both assessments had half the risk of developing colon cancer relative to those who were inactive (less than 1000 kilocalories/wk) at both assessments (age-adjusted rate ratio = 0.50; 90% confidence interval = 0.27-0.93), whereas those who were moderately active (1000-2500 kilocalories/wk) at both assessments had an age-adjusted rate ratio of 0.52 (90% confidence interval = 0.28-0.94). We conclude that either consistently higher levels of activity are necessary to protect against colon cancer or combining two assessments increased the precision of physical activity measurement. We found no evidence that increased physical activity protected against rectal cancer.

We examined patterns of physical activity and other characteristics that might deter hypertension or delay all-cause mortality among university alumni, 1962-1985. Collegiate sports play did not alter hypertension incidence, nor did contemporary walking, stair-climbing, or light sports play among 5463 University of Pennsylvania alumni, 739 of whom developed hypertension. But vigorous sports play reduced hypertension incidence; and overweight, gain in weight, history of parental hypertension, or any combination of these, increased it. Among 819 hypertensive Pennsylvania alumni (138 died during follow-up), vigorous sports play had minimal influence on mortality; but freedom from overweight and cigarette smoking deferred death. Among 16,936 Harvard College alumni, of whom 2614 died during follow-up, lack of vigorous sports play, or presence of hypertension, cigarette smoking, and overweight increased risk of premature mortality, heightened by any combination of these adverse characteristics. Overall, we found an inverse relationship between vigorous sports participation and hypertension risk but a direct relationship between risk and weight-for-height, weight gain, or parental hypertension. With regard to all-cause mortality, cigarette smoking and hypertension were most hazardous for the individual; smoking and lack of vigorous recreational play were most hazardous for the alumnus population as a whole.

Background: Physical activity is recommended by physicians to patients with non-insulin-dependent diabetes mellitus (NIDDM), because it increases sensitivity to insulin. Whether physical activity is effective in preventing this disease is not known., Methods: We used questionnaires to examine patterns of physical activity and other personal characteristics in relation to the subsequent development of NIDDM in 5990 male alumni of the University of Pennsylvania. The disease developed in a total of 202 men during 98,524 man-years of follow-up from 1962 to 1976., Results: Leisure-time physical activity, expressed in kilocalories expended per week in walking, stair climbing, and sports, was inversely related to the development of NIDDM: The incidence rates declined as energy expenditure increased from less than 500 kcal to 3500 kcal. For each 500-kcal increment in energy expenditure, the age-adjusted risk of NIDDM was reduced by 6 percent (relative risk, 0.94; 95 percent confidence interval, 0.90 to 0.98). This association remained the same when the data were adjusted for obesity, hypertension, and a parental history of diabetes. The association was weaker when we considered weight gain between the time of college attendance and 1962 (relative risk, 0.95; 95 percent confidence interval, 0.90 to 1.00). The protective effect of physical activity was strongest in persons at highest risk for NIDDM, defined as those with a high body-mass index, a history of hypertension, or a parental history of diabetes. These factors, in addition to weight gain since college, were also independent predictors of the disease., Conclusions: Increased physical activity is effective in preventing NIDDM, and the protective benefit is especially pronounced in persons at the highest risk for the disease.

A case-control analysis of Parkinson's disease and smoking habits was conducted in a cohort of 50,002 men who attended Harvard College (Cambridge, MA) or the University of Pennsylvania (Philadelphia, PA) between 1916 and 1950 and were followed in adulthood for morbidity and mortality data. Ninety-six cases of Parkinson's disease were identified from responses to a mailed questionnaire, addressed in 1976 to the University of Pennsylvania alumni and in 1977-1978 to the Harvard alumni. Four controls from the same population were selected for each case. Even though no statistically significant association was found, the results support a negative association between cigarette smoking and Parkinson's disease.

Mortality rates among 838 white female breast cancer patients were examined for relationships to personal characteristics assessed at time of diagnosis. These included weight and body mass index, oral contraceptive use, and prior menstrual and reproductive events. Multivariate analyses were used to determine the importance of these characteristics in predicting death rates specific for age and extent of disease at time of diagnosis. Weight was associated with poor prognosis among premenopausal patients, but not among postmenopausal patients. Premenopausal women weighing more than 140 lbs at diagnosis had death rates 1.7 times those of lighter women (P = 0.04). This effect was not explained by differences in the distribution of disease stage between the two groups. Body mass index was positively associated with mortality in both premenopausal and postmenopausal patients. In the entire group, the death rate ratio was 1.4 (P = 0.02) for obese (body mass index greater than 30.4 X 10(-3) lbs/in.2) vs lean women. Among premenopausal patients, parous women had higher mortality rates than nulliparous women (death rate ratio = 2.0, P = 0.06). Although the data were sparse, death rates were higher for women having a full-term pregnancy within 2 years of diagnosis than for premenopausal women with earlier pregnancies. Oral contraceptive use, age at menarche, age at first full term birth, and age at menopause were unrelated to mortality.

Longitudinal study of 16,936 Harvard alumni, followed for life-style experiences as related to cardiovascular disease (CVD) and longevity, identified 572 first coronary heart disease (CHD) attacks, 1962-1972, and 1,413 all-cause deaths, 1962-1978. Men expending 8.4+ MJ (2,000+ kcal) per week in walking, stair-climbing, and sports play were at 39% lower risk of developing CHD than less active classmates. Attributable risk estimates suggested: there might have been 16% fewer CVD deaths in the alumni population if every man had exercised 8.4+ MJ per week; 25% fewer from total cigarette abstinence; 9% fewer from abolition of hypertension; 6% fewer with less obesity; and 11% fewer CVD deaths in the absence of parental CHD. Discounting the influence of blood pressure status, cigarette habit, net weight gain since college, and parental history of early death, the more active alumni (39% of the population) are estimated to have lived on average one and one-quarter years longer than less active men.

We examined the physical activity and other life-style characteristics of 16,936 Harvard alumni, aged 35 to 74, for relations to rates of mortality from all causes and for influences on length of life. A total of 1413 alumni died during 12 to 16 years of follow-up (1962 to 1978). Exercise reported as walking, stair climbing, and sports play related inversely to total mortality, primarily to death due to cardiovascular or respiratory causes. Death rates declined steadily as energy expended on such activity increased from less than 500 to 3500 kcal per week, beyond which rates increased slightly. Rates were one quarter to one third lower among alumni expending 2000 or more kcal during exercise per week than among less active men. With or without consideration of hypertension, cigarette smoking, extremes or gains in body weight, or early parental death, alumni mortality rates were significantly lower among the physically active. Relative risks of death for individuals were highest among cigarette smokers and men with hypertension, and attributable risks in the community were highest among smokers and sedentary men. By the age of 80, the amount of additional life attributable to adequate exercise, as compared with sedentariness, was one to more than two years.

To appraise the role of physical activity in reducing coronary mortality among longshoremen, 6351 men, 35 to 74 years old upon entry, were followed for 22 years or to death or to the age of 75. Their longshoring experience was computed in terms of work-years according to categories of high, medium and low caloric output. Individual work assignments were reclassified annually to allow for effect of job transfers. The age-adjusted coronary death rate for the high-activity category was 26.9 per 10,000 work-years, and the medium and low catgories had rates of 46.3 and 49.0 which were little different from each other. This protective "threshold" effect was seen especially for the sudden-death syndrome, in which the death rate for heavy workers was 5.6, as contrasted with 19.9 for moderate and 15.7 for light workers. We conclude that repeated bursts of high energy output established a plateau of protection against coronary mortality, and that several different mechanisms may explain this finding.

Several studies are reviewed that examine the role of exercise in men at work and in men at leisure activity and sports play. All show that adequate exercise reduces the risk of coronary heart disease. Many recent investigations have undertaken the study of the various mechanisms by which physical activity produces these effects.

We conducted a case-control study to search for any relationship between use of oral contraceptives and development of breast cancer or benign breast disease. Women less than 50 years old with these diseases were matched with 2 controls by age, race, religion, and hospital. Home interviews elicited information on oral contraceptive use and other host and environmental factors. The study population comprised 1,770 women, including 452 with breast cancer and 446 with benign breast disease. The relative risk of developing cancer or benign disease was measured by matched set and summary chi-square analyses. Although the relative risk of developing breast cancer among "ever-users" of oral contraceptives was 1.1, the risk among women using oral contraceptives for 2-4 years was 1.9 (significantly increased). This risk estimate reached 2.5 for the 2- to 4-year users if they were still taking oral contraceptives when entered into study. Moreover, prior biopsy for benign breast disease increased the cancer risk among long-term users by as much as 11-fold. The relative risk of breast cancer did not vary by age, interval since first use, earliest year of use, or interval since last use. These results could be interpreted to indicate that oral contraceptives did not induce breast cancer but may have accelerated the growth rate of preexisting breast cancer. The relative risk of developing benign breast disease among ever-users of oral contraceptives was 0.8 (significantly reduced); it decreased with longer duration of use until it reached 0.2 for women who took these hormones 8 years or more. The relative risk of benign breast was not affected by earliest year of use or interval since last use. We concluded that oral contraceptives reduced the incidence of benign breast disease, but that use of steroid hormones is ill-advised for women with already established benign breast disease.

The Workshop on Epidemiologic and Public Health Aspects of Physical Activity and Exercise was conducted by the Centers for Disease Control on September 24-25, 1984. Fundamental topics were identified prior to the workshop, and experts were invited to participate. Ten papers were written, discussed at the workshop, revised, and are herewith published. The beneficial effects of physical activity on health are becoming progressively more apparent. A reduced risk of coronary heart disease, desirable weight control, and the reduction of symptoms of anxiety and mild to moderate depression are established. Beneficial effects on hypertension, type II diabetes, osteoporosis, and certain psychiatric and psychologic conditions appear likely but require additional study. Although the importance of physical activity to health is becoming better established, several important gaps in our knowledge remain. Physical activity is a complex behavior that is difficult to measure, and the accuracy of most measurement instruments is not known. Knowledge of the patterns of physical activity within our society and the determinants of those patterns is limited. Information on the rates of mechanical, metabolic, and psychologic risks of physical activity is largely absent. In addition, there is a need to know more about the dose-response effects of physical activity, the differential effects on various subgroups of the population, the specific dimensions of activity which effect different aspects of health, and the efficacy of various intervention and promotional strategies. Each paper stands as an independent contribution to the literature. As a group, the authors of these papers have provided the public health and scientific communities with a succinct yet comprehensive summary of the status of knowledge plus specific recommendations for future research in the areas of physical activity, public health, and epidemiology.

Urine specimens from 94 premenopausal women with breast cancer and from 70 control women have been compared with respect to concentration of the three major estrogen fractions and to frequency of ovulation as assessed by urine pregnanediol. The probability of anovulation (0.14 in the breast cancer patients and 0.09 among the controls) was not significantly higher among the women with breast cancer (P approximately 0.30). However, there was a positive association between urine estrogen concentration and breast cancer risk. The association was statistically significant (P less than 0.05) for each of the three estrogens measured and in both the follicular and the luteal phases of the menstrual cycle; the relative risk increased from 1 in the referent category (less than 5 micrograms estrogen/g creatinine) to about 3 in the highest category (greater than or equal to 15 micrograms estrogen/g creatinine). The association between urine estrogens and breast cancer risk was consistently stronger when the comparison was restricted to specimens collected in menstrual cycles during which ovulation occurred.

Population surveys have demonstrated an inverse relationship between breast cancer incidence rates and the urine "estriol ratio," the concentration of estriol relative to the sum of the concentrations of estrone and estradiol. In this study, the urine estriol ratio was evaluated in premenopausal breast cancer patients and control women from Boston and San Francisco. Although at least 2 years had passed since last use of oral contraceptives, women with a history or oral contraceptive use for 19 months or longer excreted estrogen in low concentrations compared to nonusers and so were excluded. Among the remaining 73 cases and 55 controls, the cases had lower estriol ratios and higher estrone and estradiol levels than did controls. However, these differences, which averaged about 10%, were not statistically significant. Thus the hypothesis that a low estriol ratio is a cause of breast cancer is given only minimal support. Among women in their 40's, the excretion of estrogens is subject to many influences and is difficult to study. The many determinants of estrogen excretion, including age and oral contraceptive use, should be accommodated in the design of future studies of the estriol ratio.

The relation of resting heart rate on biennial ECG examinations to mortality rates over 30 years of follow-up of the Framingham cohort was examined based on 1876 total deaths and 894 cardiovascular deaths, evolving out of 5070 subjects free of cardiovascular disease at entry into the study. In both sexes, at all ages, all-cause, cardiovascular, and coronary mortality rates increased progressively in relation to antecedent heart rates determined biennially. A more impressive association to cardiovascular disease was observed in men than in women, which was independent of associated cardiovascular risk factors. Case fatality rates following coronary events also increased with antecedent heart rate and the fraction of coronary deaths as sudden death increased strikingly with heart rate in men 35 to 64 years of age. There was also a substantial excess of noncardiovascular deaths at high heart rates, and the proportion of all deaths resulting from cardiovascular disease did not increase with heart rate. The excess cardiovascular deaths with more rapid heart rates were also noted, excluding those with interim overt cardiovascular disease, suggesting an effect independent of preexisting cardiac damage.

From college data on 50,000 male former students, the records of 126 men who died of pancreatic cancer in a 16-50 yr follow-up period were compared with those of 504 surviving classmates with respect to physical and social characteristics. Return mail questionnaires received from 30,000 surviving alumni in 1962 or 1966 also were reviewed for characteristics that might predict altered risk of pancreatic cancer. Strong positive associations were found for cigarette smoking as reported both during college (p less than 0.001) and at time of questionnaire return (p = 0.03). Smoking 10 or more cigarettes per day during college corresponded to a relative risk of 2.6 with 95% confidence limits 1.5 to 4.6, and a positive smoking history at questionnaire return yielded a relative risk of 2.4 (1.1-5.1). No association was found for collegiate coffee drinking, either before or after adjustment for cigarette smoking. The relative risk for coffee drinking adjusted for smoking was 1.1 (0.7-1.8). In contrast, collegiate tea consumption was associated with a reduction in pancreatic cancer risk. The relative risk for tea drinking adjusted for smoking was 0.5 (0.3-0.9). Men who at college physical examination complained of occasional abdominal pain or discomfort had increased relative risk of pancreatic cancer (3.1 : 1.1-9.0) in the follow-up period.

From the college entrance health data of 50,000 male former students, the records of 45 who eventually died of Hodgkin's disease were compared with those of 180 surviving classmates with reference to certain indicator characteristics. Risk ratios of Hodgkin's disease tended to be lower for men who had experienced various common contagious diseases in childhood. This reduced incidence of clinical contagions may signify that: 1) Inadequate early challenge of immune mechanisms left subjects more susceptible to later Hodgkin's disease, whether or not it is of infectious origin; 2) heightened immune mechanisms that led to subclinical attacks of early contagious diseases promoted an autoimmune response that evolved as Hodgkin's disease; or 3) early childhood infections eliminated some subjects who otherwise would have attended college and ultimately developed adult-onset Hodgkin's disease. Also, Hodgkin's disease risk was higher for students who had reported early death of a parent, particularly from cancer. Moreover, the risk tended to be increased among collegians who were obese, heavy cigarette smokers, and coffee drinkers. None of these indicator characteristics was associated with 89 fatal lymphomas of other types that occurred in the same study population.

Physical and social characteristics recorded at college physical examination or reported at subsequent alumni questionnaire in 1962 or 1966 by 47,271 male former students from Harvard University and the University of Pennsylvania were reviewed for their relationship to risk for cancers of the kidney, bladder, prostate and testis. The records of 213 subjects who died with 1 of these cancers in a 16-50 year followup period and of 280 subjects who reported such a cancer by mail questionnaire in 1976 or 1977 were compared with those of 1,972 matched classmates who were known to be alive and cancer-free at the time subjects with cancer had died or were diagnosed. Students with a record of proteinuria at college physical examination experienced increased risk of kidney cancer. Higher levels of body weight during college were associated with elevated risks of kidney and bladder cancers; however, increased weight in 1962/1966 related only to kidney cancer. A history of cigarette smoking as reported by questionnaire in 1962/1966 predicted increased occurrence of bladder cancer. Students with a history of tonsillectomy at college entrance experienced increased risk of prostate cancer, and those who reported cancer history in 1 or both parents were at increased risk for testicular cancer. These and other findings are presented as clues deserving further exploration for any etiological significance they may hold for the cancer sites studied.

Epidemiological studies have left no doubt as to the existence of a strong inverse relationship between physical exercise and coronary heart disease (CHD) risk. British studies of transport workers and civil servants, together with American studies of stevedores and college alumni, have provided persuasive evidence that contemporary vigorous activity is accompanied by lower risk of both fatal and nonfatal CHD. The relationship is largely independent of influential characteristics of high risk such as cigarette smoking, hypertension, obesity, and family history of hypertensive--atherosclerotic disease. Recent studies of occupational or leisure physical exercise among residents of Framingham, Massachusetts, the state of Iowa, four residential areas of Holland, urban--rural sections of Puerto Rico, Seattle--King County, Washington, city employees in Los Angeles, and various regions of Finland and Norway support the likelihood that the inverse relationship of exercise and CHD is causal, signifying a protective effect of exercise rather than an incidental contrast due to a selective influence of precursive CHD symptoms. Experimental studies in monkeys have added laboratory evidence that endurance exercise inhibits the development of CHD. The questions we need to address are not whether exercise is a real element for cardiovascular health, but what kind of exercise is needed, and how much, i.e., with what frequency, intensity, timing, and duration. An understanding of the ways and means by which exercise alters CHD risk is only beginning to emerge, but there is wide acceptance that its benefits are vitally needed in the sedentary Western world.

A preliminary analysis of data from 1,477 patients with breast cancer and 2,695 control women examined potential characteristics of high risk for breast cancer to determine whether prediction differed depending on whether the women were premenopausal, paramenopausal (intermediate), or postmenopausal. Since information was not yet available on real or presumed menopausal status, women were characterized by age: women less than 45 years as premenopausal; women from 45 through 54 years as paramenopausal; and women 55 years and older as postmenopausal. Height, weight at age 20, number of stillbirths, number of abortions, and history of cancer of any site in the subject's mother did not affect the risk of breast cancer. Generally, highest level of education, number of pregnancies, and number of live births seemed to predict risk of breast cancer. Weightbody mass index, age at menarche, and age at first pregnancy may predict breast cancer risk differently depending on the menopausal stage in which onset occurs.

Physical and social characteristics recorded at college physical examination and reported in subsequent questionnaires to alumni in 1962 or 1966 by 50,000 former students from Harvard University and the University of Pennsylvania were reviewed for their relationship to major site-specific cancer occurrence. The records of 1,359 subjects who died with a major site-specific cancer in a 16- to 50-year follow-up period and of 672 subjects who reported such a cancer by mail questionnaire in 1976 or 1977 were compared with those of 8,084 matched classmates who were known to be alive and free of cancer at the time subjects with cancer had died or had been diagnosed. Cigarette smoking, as reported both in student years and years as alumni, predicted increased risk for cancers of the respiratory tract, pancreas, and bladder. Student coffee consumption was associated with elevated risk for leukemia, but it was unrelated to cancers of the pancreas and bladder. Male students with a record of proteinuria at college physical examination experienced increased risk of kidney cancer, and those with a history of tonsillectomy experienced increased risk of prostate cancer. Students who at college entrance reported occasional vague abdominal pain were at elevated risk for pancreatic and colorectal cancers in later years. Increased body weight during college was associated with increased risks of kidney and bladder cancers, whereas for alumni this index was associated only with kidney cancer. Increased weight-for-height during college (but not in 1962 or 1966) predicted increased occurrence of female breast cancer. Jewish students experienced elevated risk for subsequent cancers of the female breast, colon, and combined colorectum. These and other findings are presented as clues deserving further exploration for any etiologic significance that they may hold for the cancer sites studied.