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Obesity has been associated with an increased risk of cancer at a number of sites. A notable exception appears to be lung cancer, for which several studies suggest a modest inverse association. However, cigarette smoking is directly associated with lung cancer and inversely associated with body mass index. To investigate the hypothesis that body mass index is associated with lung cancer independent of cigarette smoking, the authors analyzed data from a prospective cohort study of 41,837 Iowa women aged 55-69 years at baseline in 1986. In addition, they examined whether central adiposity (high waist/hip ratio) was associated with lung cancer incidence. Through 1992 (6 years of follow-up), 233 cases of lung cancer were identified through the State Health Registry of Iowa. The body mass index at several ages was calculated from self-reports of height at baseline and weights at ages 18, 30, 40, and 50 years and at baseline. Current and former smokers generally had lower mean body mass indices than did nonsmokers at all ages except 18 years. Cases generally had lower body mass indices than did noncases at all ages except 18 and 30 years but, among current smokers, cases had higher mean body mass indices than did noncases at all ages except baseline, although the differences were not statistically significant. An apparent positive association of a high waist/hip ratio with lung cancer in the total cohort was found to be primarily accounted for by a higher waist/hip ratio in current and former smokers. When stratified by smoking status and adjusted for other risk factors, including age and pack-years of smoking, the body mass index at baseline, body mass index at age 50 years, and waist/hip ratio were not associated with lung cancer. The results of multivariate analyses suggest that the inverse association of body mass index with lung cancer can be explained by smoking status and that the positive association of waist/hip ratio with lung cancer can be explained by pack-years of smoking.

Noninsulin-dependent diabetes mellitus and postmenopausal breast cancer share a number of risk factors, including obesity, increased waist-to-hip ratio, and a positive family history. If risk for these diseases is mediated through a familial tendency for abdominal obesity, then one might expect to see familial clustering of both diseases. We analyzed data from a prospective cohort study of 41,837 Iowa women age 55-69 years. Diabetes was not associated with incidence of breast cancer [relative risk (RR) = 0.97]. The association between family history of breast cancer and breast cancer incidence, however, was slightly modified by individual history of diabetes: a positive family history of breast cancer in the absence of baseline diabetes was associated with a relative risk of 1.36 [95% confidence interval (CI) = 1.08-1.70], whereas the presence of both factors was associated with a RR of 1.87 (95% CI = 0.93-3.76). Adjustment for waist-to-hip ratio greatly diminished this difference. Conversely, a family history of breast cancer was associated with a RR of 5-year diabetes mortality of 1.94 (95% CI = 1.17-3.24) that persisted after stratification by tertile of waist-to-hip ratio. No clear association of family history of breast cancer and waist-to-hip ratio for self-reported diabetes incidence was evident. These data are indicative of a complex interrelation between waist-to-hip ratio, familial predisposition, diabetes, and breast cancer.

The aggregation of colon, endometrial, ovarian, and possibly breast cancers in families has been described as a "cancer family syndrome" (now called Lynch syndrome II). To determine if the familial clustering of these malignancies was more common in women with cancer than without, we analyzed data from the Iowa Women's Health Study (IWHS), a population-based sample of 41,837 women aged 55-69 years. Self-reported information was collected on history of colon, uterine, ovarian, and breast cancers in female first-degree relatives. A family history of cancer of the breast (odds ratio [OR] = 1.4), colon (OR = 1.3), and uterus (OR = 1.3), but not ovary (OR = 1.2), was significantly more common among women with a personal history of any of these four cancers (all P < 0.05); the pattern of the ORs suggested strongly that the clustering tended to be site-specific. Age-adjusted relative risks (RR) of incident colon cancer over 5 years of follow-up (N = 237) were calculated with regard to family history. Colon cancer incidence was increased among women with a family history of breast (RR = 1.3), uterine (RR = 1.4), colon (RR = 1.5), and ovarian (RR = 1.3) cancers, although none of the risk estimates achieved statistical significance. RR was, however, significantly related to the number of different cancer sites reported among family members (Ptrend = 0.008). These data on a representative sample of postmenopausal women suggest that family histories of colon, breast, uterine, and ovarian cancers are associated with an increased risk of cancer at the same site, but provide little support for the hypothesis that Lynch syndrome II is a non-random occurrence.

Background: Although the results of animal studies and cross-cultural comparisons generally support a role for dietary fat in the etiology of breast cancer, results of analytic epidemiology studies are equivocal., Purpose: The association between dietary fat and subsequent breast cancer was examined in a cohort of 34,388 postmenopausal women from Iowa., Methods: Dietary habits were assessed by a food-frequency questionnaire mailed in January 1986. Through December 31, 1989, 459 incident cases of breast cancer occurred in this cohort. Proportional hazards regression was used to examine the dietary fat-breast cancer association while adjusting for potential confounders. The effects on this association of four analytic approaches to adjustment for energy intake were also considered., Results: After adjustment for known determinants of breast cancer, a modest positive association of total fat intake with risk of breast cancer was seen. Polyunsaturated fat intake was also positively associated with breast cancer (relative risk from lowest to highest intake, 1.0, 1.25, 1.31, and 1.49; P for trend = .052). Different approaches to adjustment for energy intake, however, provided different impressions of the dietary fat-breast cancer association. One method, involving categorization of crude fat intake and inclusion of total energy intake in regression analysis, gave relative risk estimates from low to high fat intake of 1.0, 1.17, 1.25, and 1.38 (P for trend = .18). Another method, based on categorization of fat intake residuals in which the variation in fat due to total energy intake was removed, gave corresponding estimates of 1.0, 1.24, 1.30, and 1.16 (P for trend = .29). The former suggests increasing breast cancer risk with increasing fat intake; the latter suggests no association., Conclusions: These results are consistent with other cohort studies that have shown a weak association or no association between dietary fat and breast cancer. They are also consistent with studies suggesting that fat intake is a determinant of breast cancer, particularly after accounting for inaccuracies in dietary assessment. The effects of different energy-adjustment methods may account in part for the varying interpretations of four previous cohort studies of dietary fat and breast cancer., Implications: Further work is needed to clarify not only the nature of the dietary fat-breast cancer association, but also the impact of different analytic methods used in the investigation of diet-disease associations.