Biomedical subjects

L H Kushi

Publications and source records attributed to L H Kushi.

At least 37 records · Page 2Linked to original sources

PubMed2000

Association of diet and mammographic breast density in the Minnesota breast cancer family cohort.

Mammographic breast density is a significant risk factor for breast cancer. The present report analyzes the association of breast density and dietary factors in 1508 women in a historical cohort study of breast cancer families in Minnesota. Diet was assessed by a semiquantitative food frequency questionnaire. Percent breast density was estimated visually by a radiologist experienced in mammography. The association of percent breast density with quartiles of energy-adjusted dietary intakes was examined in analysis of covariance models adjusting for potential confounding effects of age, body mass index, and other covariates as well as correcting for familial correlation. Analyses were performed on all women combined and were also stratified by menopausal status. Among premenopausal women, percent breast density was positively associated with intakes of polyunsaturated fat, polyunsaturated:saturated fat ratio, and vitamins C and E and was inversely associated with saturated fat and total dairy intake. Among postmenopausal women, vitamin B12 was linearly associated with increased breast density. The positive associations for vitamin C and B12 were attributable to supplement intake only. There was a suggestive positive trend between breast density and daily alcohol consumption in both premenopausal and postmenopausal women. After adjustment for other sources of alcohol, only wine intake among postmenopausal women was significant such that white wine showed a positive association and red wine an inverse association with percent breast density. There was no association with other examined dietary factors. The cross-sectional differences in breast density across levels of dietary factors were small in magnitude but may have implications for breast cancer risk.

Adult↗

PubMed1999

Dietary flavonoid intake and risk of cardiovascular disease in postmenopausal women.

Flavonoids, a group of phenolic compounds found in fruits and vegetables, are known to have antioxidant properties. They prevent low density lipoprotein oxidation in vitro and thus may play a role in the prevention of coronary heart disease (CHD). In 1986, in a prospective study of 34,492 postmenopausal women in Iowa, the authors examined the association of flavonoid intake with CHD and stroke mortality. Over 10 years of follow-up, 438 deaths from CHD and 131 deaths from stroke were documented. Total flavonoid intake was associated with a decreased risk of CHD death after adjusting for age and energy intake (p for trend = 0.04). This association was attenuated after multivariate adjustment. However, decreased risk was seen in each category of intake compared with the lowest. Relative risks and 95% confidence intervals of CHD death from lowest to highest intake category were 1.0, 0.67 (95% confidence interval (CI) 0.49-0.92), 0.56 (95% CI 0.39-0.79), 0.86 (95% CI 0.63-1.18), and 0.62 (95% CI 0.44-0.87). There was no association between total flavonoid intake and stroke mortality (p for trend = 0.83). Of the foods that contributed the most to flavonoid intake in this cohort, only broccoli was strongly associated with reduced risk of CHD death. The data of this study suggest that flavonoid intake may reduce risk of death from CHD in postmenopausal women.

Aged↗

PubMed1999

Relation of calcium, vitamin D, and dairy food intake to ischemic heart disease mortality among postmenopausal women.

To investigate whether greater intakes of calcium, vitamin D, or milk products may protect against ischemic heart disease mortality, the authors analyzed data from a prospective cohort study of 34,486 postmenopausal Iowa women 55-69 years old and without a history of ischemic heart disease who completed a dietary questionnaire in 1986. Through 1994, 387 deaths due to ischemic heart disease were documented (International Classification of Diseases, Ninth Revision, codes 410-414, 429.2). The multivariate-adjusted relative risks for the highest versus the lowest quartiles of total calcium, vitamin D, and milk product intakes were as follows: 0.67 (95% confidence interval (CI) 0.47-0.94; p for trend = 0.09) for calcium, 1.41 (95% CI 0.93-2.15; p for trend = 0.12) for vitamin D, and 0.94 (95% CI 0.66-1.35; p for trend = 0.68) for milk products. The relative risk was 0.63 (95% CI 0.40-0.98) for high dietary calcium but no supplemental calcium intake and 0.66 (95% CI 0.36-1.23) for high supplemental calcium but low dietary calcium intake. These results suggest that a higher intake of calcium, but not of vitamin D or milk products, is associated with reduced ischemic heart disease mortality in postmenopausal women, and reduced risk may be achievable whether the higher intake of calcium is attained by diet, supplements, or both.

Aged↗

PubMed1999

Prospective study of diet and ovarian cancer.

Evidence on dietary risk factors for ovarian cancer is inconsistent, but some studies have suggested positive associations with dietary fat, lactose, and cholesterol and negative associations with green and yellow vegetable intake. By using information from the Iowa Women's Health Study, the authors investigated the association of epithelial ovarian cancer with dietary factors in a prospective study of 29,083 postmenopausal women. Dietary information was ascertained via a food frequency questionnaire mailed to participants in 1986. During 10 years of follow-up (1986-1995), 139 of the women developed incident epithelial ovarian cancer. Incidence of the disease was not associated with dietary fat intake. Lactose and cholesterol showed moderately elevated risks. Multivariable-adjusted relative risks for the lowest to highest quartiles of lactose intake were 1.00, 1.38, 1.25, and 1.60 (p for trend = 0.12). For cholesterol, the corresponding values were 1.00, 1.34, 1.86, and 1.55 (p for trend = 0.06). Consumption of eggs was also associated with an increased risk of ovarian cancer. Multivariable-adjusted relative risks for increasing frequency of egg consumption were 1.00 (<1/week), 1.12 (1/week), 2.04 (2-4/week), and 1.81 (>4/week) (p for trend = 0.04). Total vegetable intake was modestly and inversely associated with the risk of ovarian cancer (p for trend = 0.21). Green leafy vegetable intake was more strongly associated with a decreased risk: multivariable-adjusted relative risks for the lowest to highest intake levels were 1.00, 0.80, 0.87, and 0.44 (p = 0.01). These findings are generally in agreement with the results from previous, mostly case-control studies of diet and epithelial ovarian cancer.

Aged↗

PubMed1999

Inclusion of risk factor covariates in a segregation analysis of a population-based sample of 426 breast cancer families.

Although many segregation analyses of breast cancer have been published, few have included risk factor covariates. Maximum likelihood segregation analyses examining age-at-onset (model 1) and susceptibility (model 2) models of breast cancer were performed on 426 four-generation families originally ascertained between 1944 and 1952 through a breast cancer proband. Cancer status and risk factor data were collected through interviews of participants or surrogates. When segregation analyses were performed on 10,791 women, without estimation of any covariates, all hypotheses under both models were rejected. Model 1, which required estimation of fewer parameters than model 2, provided a better fit to the data according to Akaike's Information Criterion. Further segregation analyses were performed under model 1 on a subset of women with complete data on education, age at first birth (nulliparous women included), and alcohol use, covariates that were found to significantly (P<0.05) improve the fit over the addition of exam age alone in logistic regression models. All three covariates improved the fit of the models, as did year of birth, but at all stages of model building, all of the hypotheses were still rejected. After the allele frequency was fixed at 0.0033, a subset of families appeared to fit a dominant model. Using this model, risk estimates were calculated based on inferred genotype, age, and covariate values. The penetrance was estimated to be 0.15, much lower than previous estimates based on families ascertained through breast cancer probands with early onset. Moreover, the estimates of penetrance were not greatly influenced by incorporation of the measured risk factors.

Adult↗

PubMed1999

Vitamin E and heart disease: a case study.

The role of nutritional epidemiology studies in the development of nutritional recommendations has been controversial, in part because individual studies supporting either side of a given issue can often be identified. Several sets of criteria for inference of a causal relation between a dietary factor and a disease from epidemiologic studies have been suggested. One such set is that of Sir Austin Bradford Hill, which includes criteria such as strength of association, dose-response relation, consistency of association, temporally correct association, specificity of association, and biological plausibility. Another set of criteria, used by the US Preventive Services Task Force, ranks evidence according to study design, designating evidence from randomized controlled trials as superior to evidence from cohort or case-control studies, which are in turn superior to evidence from ecologic studies or opinions of respected authorities. The application of these criteria to the question of whether vitamin E intake is associated with coronary heart disease is examined here. It is suggested that the epidemiologic evidence from prospective cohort studies generally supports an inverse association of vitamin E intake and risk of coronary heart disease. The information available from randomized trials is limited but suggestive of an inverse association with nonfatal, but not with fatal, coronary events. It is suggested that the application of criteria for causal inference to specific questions in nutritional epidemiology may provide clarity to seemingly contradictory information.

Causality↗

PubMed1999

Cereals, legumes, and chronic disease risk reduction: evidence from epidemiologic studies.

There is growing evidence that cereals and legumes play important roles in the prevention of chronic diseases. Early epidemiologic studies of these associations focused on intake of dietary fiber rather than intake of grains or legumes. Generally, these studies indicated an inverse association between dietary fiber intake and risk of coronary artery disease; this observation has been replicated in recent cohort studies. Studies that focused on grain or cereal intake are fewer in number; these tend to support an inverse association between intake of whole grains and coronary artery disease. Studies on the association of dietary fiber with colon and other cancers have generally shown inverse relations, but whether these relations are attributable to cereals, other fiber sources, or other factors is less clear. Although legumes have been shown to lower blood cholesterol concentrations, epidemiologic studies are few and inconclusive regarding the association of legumes with risk of coronary artery disease. It has been hypothesized that legumes, in particular soybeans, reduce the risk of some cancers, but epidemiologic studies are equivocal in this regard. Overall, there is substantial epidemiologic evidence that dietary fiber and whole grains are associated with decreased risk of coronary artery disease and some cancers, whereas the role of legumes in these diseases appears promising but as yet inconclusive.

Chronic Disease↗

PubMed1999

Is whole grain intake associated with reduced total and cause-specific death rates in older women? The Iowa Women's Health Study.

OBJECTIVES: This study sought to determine whether nutrient-rich whole grains reduce mortality risk. METHODS: The study included 38,740 Iowa women, aged 55 to 69 years. A food frequency questionnaire was used to obtain data on grain intake. RESULTS: Median whole grain intake quintiles ranged from a median of 0.2 to more than 3 servings per day. Women with higher intakes had healthier lifestyles and less baseline disease. The total death rate decreased in increasing quintiles, and the pattern repeated for cancer, cardiovascular disease, and other causes combined. Adjusted for lifestyle and baseline disease, the relative hazard rate ratio for total death was about 0.85 in daily consumers of whole grain. Findings persisted in strata of baseline healthy and diseased and were not explained by dietary fiber. Rates of total mortality, but not cardiovascular disease mortality, were higher among frequent consumers of refined grain. CONCLUSIONS: Total mortality risk was inversely associated with whole grain intake and positively associated with refined grain intake. Refined grains contributed more than 20% of energy intake, and whole grains contributed 1%. Substitution of whole for refined grain may reduce chronic disease risk in the United States.

Aged↗

PubMed1999

Fifty-year follow-up of cancer incidence in a historical cohort of Minnesota breast cancer families.

A family history of breast cancer is well established as a risk factor for the disease. Because family history is a dynamic rather than a static characteristic, longitudinal studies of entire families can be very instructive in quantifying the significance of risk classification. The Minnesota Breast Cancer Family Study is a historical cohort study of relatives of a consecutive series of 426 breast cancer cases (probands) identified between 1944 and 1952. The incidence of cancer and the measurement of risk factors in sisters, daughters, granddaughters, nieces, and marry-ins was determined through telephone interviews and mailed questionnaires. Ninety-eight percent of eligible families were recruited, and 93% of members participated. A total of 9073 at-risk women were studied: 56% were biological relatives of the case probands, whereas the others were related through marriage. Through 1996, 564 breast cancers were identified in nonprobands. Compared to the rate of breast cancer among marry-ins (188 cases), sisters and daughters of the probands were at a 1.9-fold greater age-adjusted risk (128 cases; 95% confidence interval, 1.4-2.4); granddaughters and nieces were at a 1.5-fold greater risk (248 cases, 95% confidence interval, 1.2-1.8). The breast cancer risk since 1952 was not distributed equally across families: although all biological relatives had a family history of breast cancer, 166 families (39%) experienced no additional cases. Most of the cases occurred among a subset of families: 21 families had 5 breast or ovarian cancers, 8 had 6, 2 had 7, and 4 had > or =8. There was no evidence of significantly increased risk for cancer at other sites, including the ovaries, cervix, uterus, colon, pancreas, stomach, or lymphatic tissue, although there was some evidence that stomach cancer in previous generations may help define the susceptible subset. These families contain four to five generations of validated occurrences of cancer, thus minimizing the uncertainty of genetic risk inherent in a disease with a late and variable age at onset. The patterns of breast cancer in these multigeneration families is consistent with the influence of autosomal dominant susceptibility in a subset, low penetrance genes in another, and purely environmental influences in the remainder.

Adolescent↗

PubMed1998

Well-done meat intake and the risk of breast cancer.

BACKGROUND: Heterocyclic amines, mutagens formed in meats cooked at high temperatures, have been demonstrated as mammary carcinogens in animals. We conducted a nested, case-control study among 41836 cohort members of the Iowa Women's Health Study to evaluate the potential role of heterocyclic amines and intake of well-done meat in the risk for human breast cancer. METHODS: A questionnaire was mailed to individuals in the cohort who had breast cancer diagnosed during the period from 1992 through 1994 and a random sample of cancer-free cohort members to obtain information on usual intake of meats and on meat preparation practices. Color photographs showing various doneness levels of hamburger, beefsteak, and bacon were included. Multivariate analysis was performed on data from 273 case subjects and 657 control subjects who completed the survey. RESULTS: A dose-response relationship was found between doneness levels of meat consumed and breast cancer risk. The adjusted odds ratios (ORs) for very well-done meat versus rare or medium-done meat were 1.54 (95% confidence interval [CI]=0.96-2.47) for hamburger, 2.21 (95% CI=1.30-3.77) for beef steak, and 1.64 (95% CI=0.92-2.93) for bacon. Women who consumed these three meats consistently very well done had a 4.62 times higher risk (95% CI=1.36-15.70) than that of women who consumed the meats rare or medium done. Risk of breast cancer was also elevated with increasing intake of well-done to very well-done meat. CONCLUSIONS: Consumption of well-done meats and, thus, exposures to heterocyclic amines (or other compounds) formed during high-temperature cooking may play an important role in the risk of breast cancer.

Aged↗

PubMed1998

Familial correlation of dietary intakes among postmenopausal women.

A positive family history is a risk factor for many chronic diseases, including most cancers, coronary heart disease, and diabetes. Since diet is also associated with most chronic diseases, one possible explanation for non-Mendelian familial clustering is shared eating habits. Food frequency data were obtained on 3,515 sisters in the Iowa Women's Health Study, a prospective cohort of postmenopausal women. Intraclass correlations between sisters were computed on a range of energy-adjusted nutrients to determine whether dietary intakes were more similar among siblings than among unrelated individuals. Two methods were used to calculate correlations: analysis of variance modeling and weighted sibling correlations. F-tests and randomization tests were used to determine statistical significance. The intraclass correlations for all of the nutrients examined were statistically significantly greater than the hypothesized value of zero (P < 0.05). Representative correlations include dietary fiber (0.15), animal fat (0.12), vegetable fat (0.13), calcium (0.14), iron (0.04), cholesterol (0.08), sodium (0.10), vitamin D (0.16), and total energy intake (0.11). When corrected for measurement error, the magnitude of these correlations increased, on average 62%. Although modest in magnitude, these correlations may be high enough to influence familial clustering of complex diseases that are attributed, in part, to diet.

Aged↗

PubMed1998

Diet and risk of colon cancer in a large prospective study of older women: an analysis stratified on family history (Iowa, United States).

OBJECTIVE: The purpose was to investigate whether dietary associations with risk of colon cancer in women differ by family history of the disease. METHODS: Data were analyzed from a prospective cohort study of 35,216 Iowa (United States) women aged 55 to 69 years at baseline. Through 31 December 1995, 241 colon cancers were identified through record linkage with the State Health Registry. The cohort was stratified on family history of colon cancer in first-degree relatives; nutrient intakes were divided into tertiles. RESULTS: Analyses using Cox regression revealed that the association of most dietary components with colon cancer incidence were similar for individuals with and without a family history. However, total calcium intake was associated inversely with colon cancer among women with a negative family history (relative risk [RR] = 0.50 for upper cf lower tertile, P < 0.001), but was unrelated to incidence for women with a positive family history (RR = 1.1 for upper cf lower tertile, P = 0.69). Similarly, total vitamin E intake was associated with lower risk among women with a negative family history (RR = 0.67 for upper cf lower tertile, P = 0.04), but not among women with a positive family history (RR = 0.87 for upper cf lower tertile, P = 0.67). High intakes of fiber, fruits, and vegetables were each weakly inversely associated with risk among family-history negative women, but not among family-history positive women. CONCLUSIONS: These data, if corroborated, suggest that dietary factors typically associated with lower risk may be less effective risk-reduction interventions against colon cancer for individuals with a family history of colon cancer.

Age Factors↗

PubMed1998

Whole-grain intake and cancer: an expanded review and meta-analysis.

Whole grains are nutrient rich and may protect against chronic disease. To study this, we previously reviewed 14 case-control studies of colorectal, gastric, and endometrial cancers and found consistently lower risk in those with high than in those with low whole-grain intake. Questions remained concerning other cancers, dietary assessment, quantity consumed, confounding, and differential study quality. Here we expand the review to 40 case-control studies of 20 cancers and colon polyps. Odds ratios are < 1 for 46 of 51 mentions of whole-grain intake and for 43 of 45 after exclusion of 6 mentions with design/reporting flaws or low intake. The pooled odds ratio for high vs. low whole-grain intake among the 45 mentions was 0.66 (95% confidence interval = 0.60-0.72); they range from 0.59 to 0.78 across four types of dietary questionnaires. Odds ratios were < 1 in 9 of 10 mentions of studies of colorectal cancers and polyps, 7 of 7 mentions of gastric and 6 of 6 mentions of other digestive tract cancers, 7 of 7 mentions of hormone-related cancers, 4 of 4 mentions of pancreatic cancer, and 10 of 11 mentions of 8 other cancers. Most pooled odds ratios for specific cancers were in the range of 0.5-0.8, notable exceptions being breast (0.86) and prostate (0.90). The pooled odds ratio was similar in studies that adjusted for few and many covariates. Dose-response associations were stronger in studies using food-frequency questionnaires than in more quantitative questionnaires. The case-control evidence is supportive of the hypothesis that whole-grain intake protects against various cancers.

Adult↗

PubMed1998

Whole-grain intake may reduce the risk of ischemic heart disease death in postmenopausal women: the Iowa Women's Health Study.

BACKGROUND: A recent review of epidemiologic literature found consistently reduced cancer and heart disease rates in persons with high compared with low whole-grain intakes. OBJECTIVE: We hypothesized that whole-grain intake was associated with a reduced risk of ischemic heart disease (IHD) death. DESIGN: We studied 34,492 postmenopausal women aged 55-69 y and free of IHD at baseline in 1986. There were 438 IHD deaths between baseline and 1995. Usual dietary intake was determined with use of a 127-item food-frequency questionnaire. RESULTS: Whole-grain intake in median servings/d was 0.2, 0.9, 1.2, 1.9, and 3.2 for quintiles of intake. The unadjusted rate of IHD death was 2.0/1 x 10(3) person-years in quintile 1 and was 1.7, 1.2, 1.0, and 1.4 IHD deaths/1 x 10(3) person-years in succeeding quintiles (P for trend < 0.001). Adjusted for demographic, physiologic, behavioral, and dietary variables, relative hazards were 1.0, 0.96, 0.71, 0.64, and 0.70 in ascending quintiles (P for trend = 0.02). The lower risk with higher whole-grain intake was not explained by intake of fiber or several other constituents of whole grains. CONCLUSION: A clear inverse association between whole-grain intake and risk of IHD death existed. A causal association is plausible because whole-grain foods contain many phytochemicals, including fiber and antioxidants, that may reduce chronic disease risk. Whole-grain intake should be studied further for its potential to prevent IHD and cancer.

Aged↗

PubMed1998

A prospective cohort study of intake of calcium, vitamin D, and other micronutrients in relation to incidence of rectal cancer among postmenopausal women.

To investigate whether high intakes of calcium and other micronutrients (carotene, retinol, and vitamins C, D, and E) are related to reduced risks of rectal cancer, we analyzed data from a large cohort study of postmenopausal Iowa women who responded to a mailed survey in 1986. After 9 years of follow-up, 144 incident rectal cancer cases were ascertained among the 34,702 women at risk. Intake levels of micronutrients at baseline were derived from self-reported data on vitamin supplements and dietary intake of 127 foods included in a semiquantitative food frequency questionnaire. After adjustment for total energy intake and other potential confounding factors, a dose-response inverse association was observed between total calcium intake and the risk of rectal cancer: adjusted relative risks (RRs) were 1.00, 0.90, and 0.59 (trend test, P = 0.02) from the lowest to the highest calcium intake tertiles. High intakes of dietary and supplement calcium were both related to a slightly reduced risk of rectal cancer, but neither of the trend tests was statistically significant. Reduced risks of rectal cancer were also observed for high intake of carotene and vitamins A, C, and D, although none of the associations were statistically significant. For vitamin D, the adjusted RRs were 1.00, 0.71, and 0.76 (trend test, P = 0.20) for increasing intake tertiles. Compared with women who consumed low levels of both total calcium and vitamin D, those in the highest intake group of both nutrients were at a 45% reduced risk of rectal cancer (RR, 0.55; 95% confidence interval, 0.32-0.93). This study supports the hypothesis that high intake of calcium and possibly other micronutrients may be beneficial in the prevention of rectal cancer.

Aged↗

PubMed1997

The role of hormone replacement therapy in the risk for breast cancer and total mortality in women with a family history of breast cancer.

BACKGROUND: The risks and benefits of hormone replacement therapy (HRT) are of considerable interest and importance, especially in terms of whether they differ among subsets of women. OBJECTIVE: To determine whether HRT is associated with increased risks for breast cancer and total mortality in women with a family history of breast cancer. DESIGN: Prospective cohort study. SETTING: Population-based sample of midwestern post-menopausal women enrolled in an observational study of risk factors for cancer. PARTICIPANTS: Random sample of 41,837 female Iowa residents 55 to 69 years of age. MEASUREMENTS: Incidence rates of and relative risks for breast cancer (n = 1085) and total mortality (n = 2035) through 8 years of follow-up were calculated by using data from the State Health Registry of Iowa and the National Death Index. RESULTS: A family history of breast cancer was reported by 12.2% of the cohort at risk. Among women with a family history of breast cancer, those who currently used HRT and had done so for at least 5 years developed breast cancer at an age-adjusted annual rate of 61 cases per 10,000 person-years (95% CI, 28 to 94 cases); this rate was not statistically significantly higher than the rate in women who had never used HRT (46 cases per 10,000 person-years [CI, 36 to 55 cases]). Among women with a family history, those who used HRT had a significantly lower risk for total mortality than did women who had never used HRT (relative risk, 0.67 [CI, 0.51 to 0.89]), including total cancer-related mortality (relative risk, 0.75 [CI, 0.50 to 1.12]). The age-adjusted annual mortality rate for women using HRT for at least 5 years was 46 deaths per 10,000 person-years (CI, 19 to 74 deaths); this is roughly half the rate seen in women who had never used HRT (80 deaths per 10,000 person-years [CI, 69 to 92 deaths]). CONCLUSIONS: These data suggest that HRT use in women with a family history of breast cancer is not associated with a significantly increased incidence of breast cancer but is associated with a significantly reduced total mortality rate.

Aged↗

PubMed1997

Evaluation of potential sources of bias in a genetic epidemiologic study of breast cancer.

Systematic errors, or bias, can arise at several stages of a study, including selection of subjects, measurement of exposure and disease, and data analysis. Little attention appears to have been paid to potential sources of bias in genetic epidemiologic studies, despite the fact that the study of units (families) and members (relatives) within those units produces unique opportunities for bias to be introduced. The ability to evaluate whether selection bias has occurred is rare. In 1944, a case-control family study of breast cancer was initiated at the Dight Institute for Human Genetics at the University of Minnesota. A follow-up study of these 544 families is currently being conducted on sisters, daughters, nieces, and granddaughters of the probands, and a control group of women who are spouses of male first- and second-degree relatives. Updated data are collected on females who are 18 years or older through telephone interviews and questionnaires. The availability of detailed family history information on these families at baseline provided an opportunity to evaluate several potential sources of bias. Analyses were performed to determine if families lost to follow-up differed from those who were successfully located or excluded (ineligible), and whether participation rates within a family differed by relationship to proband, age, and family history of cancer. The latter participation rates for individuals were examined with respect to a telephone interview, a mailed questionnaire, and screening mammography. There were no statistically significant differences in the cancer histories of families that were excluded, those that were lost to follow-up, and those that participated. Within families, degree of relationship to the breast cancer proband was significantly associated with age-adjusted participation rates on mailed questionnaires (P < 0.005) and mammography (P < 0.005), but not telephone interviews (P = 0.29). After adjustment for age, marry-ins with a family history of breast cancer were not significantly more likely than marry-ins without a family history to undergo mammography (P = 0.11) or return mailed questionnaires (P = 0.74). Although non-participation is a potentially serious source of bias to a genetic epidemiologic study and the effect of variable participation rates should be explored when investigating the genetic component of a disease, it does not appear to be a problem for this particular study.

Adolescent↗

PubMed1997

Non-dietary factors as risk factors for breast cancer, and as effect modifiers of the association of fat intake and risk of breast cancer.

To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age 15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI] = 0.62-0.82); of being postmenopausal was 0.82 (CI = 0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI = 0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI = 1.22-1.75); of benign breast disease was 1.53 (CI = 1.41-1.65); of maternal history of breast cancer was 1.38 (CI = 1.14-1.67); and history of a sister with breast cancer was 1.47 (CI = 1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease; with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer risk.

Breast Neoplasms↗