We conducted a combined analysis of the original data to evaluate the consistency of 12 case-control studies of diet and breast cancer. Our analysis shows a consistent, statistically significant, positive association between breast cancer risk and saturated fat intake in postmenopausal women (relative risk for highest vs. lowest quintile, 1.46; P less than .0001). A consistent protective effect for a number of markers of fruit and vegetable intake was demonstrated; vitamin C intake had the most consistent and statistically significant inverse association with breast cancer risk (relative risk for highest vs. lowest quintile, 0.69; P less than .0001). If these dietary associations represent causality, the attributable risk (i.e., the percentage of breast cancers that might be prevented by dietary modification) in the North American population is estimated to be 24% for postmenopausal women and 16% for premenopausal women.

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Epidemiologic evidence on the relation between nutrition and stomach cancer is reviewed. Stomach cancer shows a distinct international variation and dramatic worldwide decline. These descriptive features suggest that dietary factors are important in determining the risk of stomach cancer. The authors assessed relevant data regarding specific dietary hypotheses in the etiology of stomach cancer. A negative association with fresh vegetables and fruits is highly consistent in numerous case-control studies in different populations. Both epidemiologic and experimental data suggest that vitamins C and carotenoids lower risk of stomach cancer. Evidence is sparse and inconsistent as to protective effects of vitamin E and selenium. Epidemiologic studies have not lent, and will not provide, supportive evidence for an etiologic role of nitrate intake. High salt intake has been associated with an increased risk in many case-control studies and limited cohort studies. Taken together with animal data, it is considered that high salt intake is a risk factor for stomach cancer. Both epidemiologic and experimental data are inconclusive as to whether high-starch diets confer an increased risk. Cohort studies using quantitative dietary assessment and biologic measurement of micronutrients are needed for further understanding of etiologic roles of dietary factors in the causation of stomach cancer.

The roles of the hepatitis B virus (HBV), cigarette smoking and alcohol consumption in the etiology of hepatocellular carcinoma (HCC) were examined in a case-control study involving 204 patients with HCC and 410 control subjects in Fukuoka prefecture, where HCC risk is among the highest in Japan. Information on smoking and drinking habits was obtained by a detailed interview survey, and the results were analyzed in conjunction with serum hepatitis B surface antigen (HBsAg) status after adjustment for sex, age and other possible confounding factors. Individuals positive for serum HBsAg showed a relative risk (RR) for HCC of 13.8 (95% confidence interval, Cl 5.9 to 32.5), whereas heavy drinkers experienced about a 2-fold risk increase compared with non-drinkers. Light or moderate drinkers, however, demonstrated RRs near the unity. Some risk excess was observed among ex-smokers (RR = 1.5, 95% CI 0.8 to 2.8) and current smokers (RR = 1.5, 0.8 to 2.7) compared with non-smokers, but without evidence for a dose-response relationship in terms of pack-years. Analysis among HBsAg-negative subjects revealed similar non-significant association with smoking, and there was no clear interaction between alcohol and cigarette consumption on HCC risk. Other significant risk factors included positive histories of blood transfusion (RR = 3.7, 2.2 to 6.3) and familiar liver disease (RR = 2.6, 1.6 to 4.2). Attributable risk calculations suggest that chronic HBV infection and heavy drinking may account for 17% and 13% of HCC occurrence, respectively, in this high risk area. The association of cigarette smoking with HCC was not evident in our study.

To investigate the association of alcohol intake, cigarette smoking, occupation, and other factors with the development of idiopathic osteonecrosis of the femoral head, a nationwide multicenter case-control study was conducted in Japan during 1988-1990, comparing 118 cases with no history of systemic corticosteroid use with 236 controls matched for sex, age, ethnicity, clinic, and date of initial examination. The risks of developing femoral head necrosis associated with potential risk factors were estimated by adjusted relative odds obtained by a conditional logistic regression model. The elevated relative odds were observed for occasional drinkers (relative odds = 3.2, 95% confidence interval 1.1-9.2) and regular drinkers (relative odds = 13.1, 95% confidence interval 4.1-42.5) with a significant dose-response relation (p < 0.001). For current drinkers, the relative odds were 2.8, 9.4, and 14.8 for < 320, 320-799, and > or = 800 g/week of ethanol intake, respectively. An increased risk was found for current smokers (relative odds = 4.7, 95% confidence interval 1.5-14.5), but a linear increasing trend in the cumulative effect of smoking was not evident at 20 pack-years or over. A weak but significant dose-response relation was observed for daily occupational energy consumption (p < 0.05). The present study confirmed the strong association of alcohol intake and positive association of cigarette smoking and suggested the role of heavy physical work.

This study examined interview data on personal habits (smoking, drinking and dietary histories) when collected from two sources. A sample of 300 pairs of subjects (mostly husbands and wives) was obtained from an ongoing health survey in Hawaii, and both members of each pair were interviewed separately about the habits of the husband. Care was taken that the members of each pair had no opportunity to communicate with each other between the start and completion of both interviews. The results showed remarkably good agreement in overall mean values between the two groups of respondents. In general, approximately 75% of the pairs agreed within acceptable limits on most items. There was no clear association of the degree of agreement within pairs with a variety of characteristics of the surrogate group, including age, race, level of education, family income, and duration of residence of proportion of meals eaten together with the subject. These findings are encouraging for the use of surrogate respondents in studies of personal habits where direct interviews are not always feasible, or where the use of such substitutes can improve the reppresentativeness and size of the sample.

We examined the relationship between aryl hydrocarbon hydroxylase (AHH) and the frequency of a Msp I mutation in the 3′‐flanking region of cytochrome P450 (CYP) 1A1 (Mspl polymorphism) and another mutation in exon 7 (Ile‐Val polymorphism) in 84 healthy male subjects in Fukuoka, Japan. AHH inducibility (3‐methylcholanthrene (MC)‐induced AHH activity/non‐induced AHH activity) was correlated with the MspI polymorphism (P<0.0001) and age class (P=0.015), whereas no correlation was found for the Ile‐Val polymorphism (P=0.509). Age‐adjusted AHH inducibility (mean±SE) of the predominant homozygote (genotype A), the heterozygote (genotype B) and a homozygote rare allele (genotype C) genotypes was 4.89±0.36, 4.82±0.29 and 13.61±1.44, respectively. The genotype C showed much higher AHH inducibility than genotypes A and B (P<0.001), while no significant difference was observed between genotypes A and B. Non‐induced AHH activity was also correlated with these polymorphisms. The AHH activity of a homozygous mutant Val/Val genotype (0.076±0.010 pmol/min/106 cells) was significantly higher (P<0.05) than that of the wild‐type homozygous Ile/Ile (0.044±0.004 pmol/min/106 cells) and heterozygous Ile/Val (0.047±0.007 pmol/min/106 cells) genotypes. Our study suggests that the genotypes C and Val/Val, which are more frequent in smoking‐related lung cancer, are closely related with high AHH inducibility and high non‐induced AHH activity, respectively. Thus, the positive relationship between AHH inducibility and lung cancer is supported by our study. If our results are confirmed and the assessment of genotype becomes feasible on a population basis, identification of smokers who have genetically high susceptibility to lung cancer (genotype C or Val/Val) may become important for the prevention of lung cancer.

The relation between obesity and adenomatous polyps of the sigmoid colon was investigated in male self‐defense officials who received a retirement health examination at three hospitals of the Self‐Defense Forces in Japan between January 1991 and December 1992. Body mass index (BMI) and waist‐hip circumference ratio (WHR) were used as indices of obesity. A total of 228 adenoma cases and 1484 controls with normal sigmoidoscopy were identified in 2228 men: cases having small adenomas (<5 mm in diameter) and those with large adenomas (5 mm or greater) numbered 115 and 102, respectively. Smoking, alcohol use, physical activity, rank, and hospital were controlled for by multiple logistic regression analysis. BMI and WHR were classified into four levels using the 30th, 60th, and 90th percentiles of each distribution in the control as cut‐off points. There was a significant two‐fold elevation in the overall adenoma risk among men at the highest BMI level (≥26.95) compared with those at the lowest level (<22.48), but the risk did not linearly increase: a similar increase was also noted for large adenomas. While WHR was only weakly related to the overall adenoma risk, the risk of large adenomas progressively increased with increasing levels of WHR: odds ratio (OR) 2.9 (95% confidence interval (CI) 1.4–5.9) for the highest (≥0.958) versus lowest (<0.878) levels. BMI was not materially associated with adenoma risk after additional adjustment for WHR, but a positive association between WHR and large adenomas was independent of BMI: OR 3.4 (95%CI 1.5–7.6) for the highest versus lowest levels. These findings suggest that obesity is associated with an increased risk of colon adenomas, probably with adenoma growth.