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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.

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 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.

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.

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 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.