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Purpose: To identify distinct diet trajectories after breast cancer (BC) diagnosis, and to examine the characteristics associated with diet trajectories., Methods: We analyzed 2865 Pathways Study participants who completed ≥ 2 food frequency questionnaires at the time of BC diagnosis (baseline), and at 6 and 24 months after baseline. Trajectory groups of fruit and vegetable (F/V) intake, % calories from dietary fat, and alcohol intake over 24 months were identified using group-based trajectory modeling. Associations between diet trajectories and sociodemographic, psychosocial, and clinical factors were analyzed using multinomial logistic regression., Results: Analyses identified 3 F/V trajectory groups, 4 dietary fat groups, and 3 alcohol groups. All 3 F/V trajectory groups reported slightly increased F/V intake post-diagnosis (mean increase = 0.2-0.5 serving/day), while 2 groups (48% of participants) persistently consumed < 4 servings/day of F/V. Dietary fat intake did not change post-diagnosis, with 45% of survivors maintaining a high-fat diet (> 40% of calories from fat). While most survivors consumed < 1 drink/day of alcohol at all times, 21% of survivors had 1.4-3.0 drinks/day at baseline and temporarily decreased to 0.1-0.5 drinks/day at 6 months. In multivariable analysis, diet trajectory groups were significantly associated with education (ORs: 1.93-2.49), income (ORs: 1.32-2.57), optimism (ORs: 1.93-2.49), social support (OR = 1.82), and changes in physical well-being (ORs: 0.58-0.61) and neuropathy symptoms after diagnosis (ORs: 1.29-1.66)., Conclusions: Pathways Study participants reported slightly increasing F/V and decreasing alcohol intake after BC diagnosis. Nearly half of survivors consumed insufficient F/V and excessive dietary fat. It is important to prioritize nutrition counseling and education in BC survivors.

Background: Because dietary fat has been postulated to affect obesity and estrogen levels, two important risk factors for endometrial cancer, its association with this disease has received some attention. We summarize here the current evidence for several dietary lipids., Methods: Searches were conducted to identify peer-reviewed manuscripts up to December 2006. Two cohort studies and nine case-control studies were included in meta-analyses., Results: Random-effects summary estimates for case-control studies were 1.24 (95% CI: 1.10, 1.41) per 10% kcal from total fat and 1.28 (95% CI: 1.12, 1.47) per 10 g/1,000 kcal of saturated fat. The only cohort study evaluating total fat and saturated fat did not find an association. We estimated a 35% increased risk (95% CI: 0.96, 1.90) per 150 mg/1,000 kcal of cholesterol intake, based on six case-control studies. For animal fat (per 10 g/1,000 kcal) the summary estimates were 0.78 (95% CI: 0.63, 0.96) and 1.34 (95% CI: 1.06, 1.69) for two cohort and four case-control studies, respectively., Conclusions: Case-control data suggest an increased risk for total, saturated, and animal fat. However, the limited available cohort data do not support these associations. Additional data, particularly from prospective studies, are needed before conclusions can be drawn.

Lung cancer rates are highest in countries with the greatest fat intakes. In several case-control studies, positive associations have been observed between lung cancer and intakes of total and saturated fat, particularly among nonsmokers. We analyzed the association between fat and cholesterol intakes and lung cancer risk in eight prospective cohort studies that met predefined criteria. Among the 280,419 female and 149,862 male participants who were followed for up to 6-16 years, 3,188 lung cancer cases were documented. Using the Cox proportional hazards model, we calculated study-specific relative risks that were adjusted for smoking history and other potential risk factors. Pooled relative risks were computed using a random effects model. Fat intake was not associated with lung cancer risk. For an increment of 5% of energy from fat, the pooled multivariate relative risks were 1.01 [95% confidence interval (CI), 0.98-1.05] for total, 1.03 (95% CI, 0.96-1.11) for saturated, 1.01 (95% CI, 0.93-1.10) for monounsaturated, and 0.99 (95% CI, 0.90-1.10) for polyunsaturated fat. No associations were observed between intakes of total or specific types of fat and lung cancer risk among never, past, or current smokers. Dietary cholesterol was not associated with lung cancer incidence [for a 100-mg/day increment, the pooled multivariate relative risk was 1.01 (95% CI, 0.97-1.05)]. There was no statistically significant heterogeneity among studies or by sex. These data do not support an important relation between fat or cholesterol intakes and lung cancer risk. The means to prevent this important disease remains avoidance of smoking.

Objective: To examine the associations between reported intakes of dietary fat and incident type 2 diabetes., Research Design and Methods: We studied the relation between dietary fatty acids and diabetes in a prospective cohort study of 35,988 older women who initially did not have diabetes. Diet was assessed with a food frequency questionnaire at baseline, and 1,890 incident cases of diabetes occurred during 11 years of follow-up., Results: After adjusting for age, smoking, alcohol consumption, BMI, waist-to-hip ratio, physical activity, demographic factors, and dietary magnesium and cereal fiber, diabetes incidence was negatively associated with dietary polyunsaturated fatty acids, vegetable fat, and trans fatty acids and positively associated with omega-3 fatty acids, cholesterol, and the Keys score. After simultaneous adjustment for other dietary fat, only vegetable fat remained clearly related to diabetes risk. Relative risks across quintiles of vegetable fat intake were 1.00, 0.90, 0.87, 0.84, and 0.82 (P = 0.02). Diabetes risk was also inversely related to substituting polyunsaturated fatty acids for saturated fatty acids and positively correlated to the Keys dietary score., Conclusions: These data support an inverse relation between incident type 2 diabetes and vegetable fat and substituting polyunsaturated fatty acids for saturated fatty acids and cholesterol.

Recently, there has been interest in whether intakes of specific types of fat are associated with breast cancer risk independently of other types of fat, but results have been inconsistent. We identified 8 prospective studies that met predefined criteria and analyzed their primary data using a standardized approach. Holding total energy intake constant, we calculated relative risks for increments of 5% of energy for each type of fat compared with an equivalent amount of energy from carbohydrates or from other types of fat. We combined study-specific relative risks using a random effects model. In the pooled database, 7,329 incident invasive breast cancer cases occurred among 351,821 women. The pooled relative risks (95% confidence intervals [CI]) for an increment of 5% of energy were 1.09 (1.00-1.19) for saturated, 0.93 (0.84-1.03) for monounsaturated and 1.05 (0.96-1.16) for polyunsaturated fat compared with equivalent energy intake from carbohydrates. For a 5% of energy increment, the relative risks were 1.18 (95% CI 0.99-1.42) for substituting saturated for monounsaturated fat, 0.98 (95% CI 0.85-1.12) for substituting saturated for polyunsaturated fat and 0.87 (95% CI 0.73-1.02) for substituting monounsaturated for polyunsaturated fat. No associations were observed for animal or vegetable fat intakes. These associations were not modified by menopausal status. These data are suggestive of only a weak positive association with substitution of saturated fat for carbohydrate consumption; none of the other types of fat examined was significantly associated with breast cancer risk relative to an equivalent reduction in carbohydrate consumption., (Copyright 2001 Wiley-Liss, Inc.)

A nutrition intervention focused on low-fat eating pattern changes was conducted among low-literacy participants in a Twin Cities Metropolitan area Expanded Food and Nutrition Education Program (EFNEP). A total of 134 EFNEP participants who participated in the intervention were compared to 70 comparison participants who received EFNEP nutrition education materials. Associations between changes in outcome variables specific to the intervention were evaluated using mixed-model regression analyses. The principal effects seen for this program were related to changes in eating pattern scales. More modest effects were seen in scales related to attitudes of low-fat eating, and although changes in dietary fat intake as measured by 24-hour dietary interviews suggested a positive intervention effect, this did not approach statistical significance.

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.

Background: The authors sought to determine whether prediagnosis obesity, body-fat distribution, and dietary intake of fats, antioxidants, and fiber may be related to survival after the diagnosis of breast cancer., Methods: The mortality rates of 698 postmenopausal patients with unilateral breast cancer in a large cohort study were analyzed. Body-mass index, waist-to-hip ratio, and food-frequency data were collected by questionnaire within 6 years before breast cancer was diagnosed., Results: Adjusted for age, women in the highest tertile of body mass index had a 1.9-fold higher risk (95% confidence interval = 1.0-3.7) of dying after breast cancer than those in the lowest tertile; adjusted for other prognostic variables (age, smoking, education level, extent of breast cancer, and tumor size), this relative risk was 1.5 (95% CI = 0.7 to 2.9). Waist-to-hip ratio was not related to risk of dying nor was intake of fiber or several dietary antioxidants. Independent of other prognostic variables, risk of death after breast cancer was statistically significantly elevated, with a relative risk greater than 2.0 for the highest tertiles of total fat, saturated fat, and monounsaturated fat intake, expressed as grams per day. An adjustment for energy intake, which also was associated positively with fatality, weakened these associations somewhat., Conclusions: Although clinical trials are required, these findings support the hypothesis that a high fat intake is associated with reduced survival of postmenopausal women with breast cancer and suggest that women with breast cancer should consider limiting their intake of fat.

The association of dietary fat with breast cancer in prospective cohort studies has generally been weak and not statistically significant. However, these studies have not considered whether the risk related to fat intake may differ according to estrogen or progesterone receptor status. Dietary habits and other breast cancer risk factors were assessed by mailed questionnaire in January 1986 in 34,388 postmenopausal Iowa women. Through 1991, 724 incident breast cancer cases were ascertained in this cohort using the Iowa cancer registry. Joint estrogen and progesterone receptor status was determined for 479 (66%) breast cancers. For tumors that were positive for both estrogen and progesterone receptors (ER+/PR+) (n = 329), age- and energy-adjusted relative risks for breast cancer adjusted from lowest to highest third of fat intake were 1.0, 1.05, and 1.22 (P trend = 0.14). Corresponding risks for ER+/PR- tumors (n = 75) were 1.0, 0.85, and 1.05 (P trend = 0.86) and for ER-/PR- tumors (n = 61) were 1.0, 1.06, and 0.73 (P trend = 0.68). Only 14 cases were classified as having ER-/PR+ tumors. Adjustment for other breast cancer risk factors did not appreciably alter these findings. There was a suggestion that dietary fat may be associated with ER+/PR+ breast cancers and not other breast cancers. These results are also consistent with an interpretation of no association between dietary fat with breast cancer, regardless of hormone receptor status. It has been suggested that etiological studies of breast cancer should investigate associations according to receptor status. This study provides evidence of a subset of breast cancers that may be related to dietary factors.(ABSTRACT TRUNCATED AT 250 WORDS)

To test the hypothesis that a high intake of dietary cholesterol and fat is associated with elevated risks of lung cancer, we analyzed data from a population-based, prospective, cohort study conducted among 41,837 postmenopausal Iowa (United States) women who completed, in 1986, a comprehensive mailed questionnaire including information on usual intake of 127 food items. All cohort members were followed for cancer incidence through the statewide cancer registry. By 1991, after six years of follow-up, 272 incident lung-cancer cases were identified. After controlling for total energy intake and other confounding factors, dietary cholesterol, total fat, and animal fat were unrelated to lung cancer risk. Intake in the upper three quartiles of plant-derived fat, however, was related to a 30 to 40 percent lower incidence of lung cancer, comparative with those in the lowest quartile, with more pronounced reduction in risk observed among smokers (relative risk = 0.6, 95 percent confidence interval = 0.4-0.9). This prospective cohort study suggests that high intake of fat of plant origin may be associated with reduced risk of lung cancer, while dietary cholesterol and animal fat intake is unrelated to the etiology of this malignancy in postmenopausal women.

To investigate the relation of dietary intakes of sucrose, meat, and fat, and anthropometric, lifestyle, hormonal, and reproductive factors to colon cancer incidence, data were analyzed from a prospective cohort study of 35,215 Iowa (United States) women, aged 55-69 years and without a history of cancer, who completed mailed dietary and other questionnaires in 1986. Through 1990, 212 incident cases of colon cancer were documented. Proportional hazards regression was used to adjust for age and other risk factors. Risk factors found to be associated significantly with colon cancer included: (i) sucrose-containing foods and beverages other than ice cream/milk; relative risks (RR) across the quintiles = 1.00, 1.73, 1.56, 1.54, and 2.00 (95% confidence intervals [CI] for quintiles two and five exclude 1.0); (ii) sucrose; RR across the quintiles = 1.00, 1.70, 1.81, 1.82, and 1.45 (CI for quintiles two through four exclude 1.0); (iii) height; RR = 1.23 for highest to lowest quintile (P for trend = 0.02); (iv) body mass index; RR = 1.41 for highest to lowest quintile (P for trend = 0.03); and (v) number of livebirths, RR = 1.59 for having had one to two livebirths and 1.80 for having had three or more livebirths compared with having had none (P for trend = 0.04). These data support hypotheses that sucrose intake or being tall or obese increases colon cancer risk; run contrary to the hypothesis that increased parity decreases risk; support previous findings of no association with demographic factors other than age, cigarette smoking, or use of oral contraceptives or estrogen replacement therapy; and raise questions regarding previous associations with meat, fat, protein, and physical activity.

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.

We examined weight changes over 1 and 2 y in 303 women enrolled in a low-fat dietary-intervention trial. Participants were randomly assigned to an intervention group that received intensive instruction in maintaining a low-fat diet or to a control group. After 1 y intervention-group women had decreased fat intake by 45.3 g (from 39.2% to 21.6% energy from fat) and weight by 3.1 kg (all P less than 0.0001); control-group women decreased fat intake by 8.8 g (from 38.9% to 37.3% energy from fat) and weight by 0.4 kg. In both univariate analyses and multivariate models, weight loss was more strongly associated with change in percent energy from fat than with change in total energy intake. These data, which are consistent with both epidemiologic and clinical studies, suggest that body adiposity is a function both of energy balance and the proportion of energy derived from fat.

A quantitative overview of 14 studies of rat colon carcinogenesis was undertaken to examine the relationship between fat intake, and fat intake by degree of saturation, on the incidence of colon carcinoma while controlling for calorie consumption. Calorie consumption was not recorded in 11 of the 14 studies. Hence, two types of analyses were conducted. The first examines carcinoma incidence as a function of percent fat (by weight), with calories controlled for by including weight gain per week in the analysis. The second estimates calories per day, for studies not providing such information, using weight gain per week and age at death, followed by a joint analysis of estimated fat calories and estimated total calories. With either approach, a rather strong positive relationship between colon carcinoma incidence and fat intake is indicated for Fischer 344 rats, but no association is apparent for Sprague-Dawley rats. This situation is somewhat clarified when the degree of saturation is taken into account: both strains gave results that suggest a negative relationship between colon cancer incidence and omega-3 fatty acids intake and a positive relationship with non-omega-3 polyunsaturated fat intake among Fischer 344 rats. These analyses suggest an important and specific role for dietary fat in the promotion of rat colon carcinoma.

The Women's Health Trial Vanguard Study was conducted to examine the feasibility of a nationwide, randomized multicenter intervention trial to test the hypothesis that a low-fat diet followed for a period of 10 years will reduce breast cancer risk. Women ages 45-69 years at increased risk of breast cancer were randomized into intervention (low-fat diet, n = 184) and control (usual diet, n = 119) groups. On the basis of 4-day food records, baseline fat intakes were comparable in the two groups, averaging 1,718 kcal with 39% of energy as fat. Intervention women reported substantially lower fat intake at 6 (20.9% kcal), 12 (21.6%), and 24 months (22.6% kcal). In contrast, control women reported only slight reductions in fat intake (37.3% kcal at 12 months and 36.8% kcal at 24 months). Evidence that these women were indeed complying with the low-fat dietary intervention comes from (a) the reasonable nature of reported nutrient changes within food groups in the intervention women and (b) agreement between observed and expected differences in plasma total cholesterol between the control and the intervention groups. At 12 months, the observed control - intervention plasma cholesterol difference was 13.1 +/- 4.6 mg/dl while the expected difference based on the Keys equation was 15.1 +/- 1.1 mg/dl; at 24 months, the observed difference was 15.5 +/- 4.3 mg/dl and the expected difference was 12.0 +/- 1.2 mg/dl. These analyses indicate that the intervention women made substantial dietary changes and have successfully maintained these changes over a 2-year period. This study thus demonstrates the feasibility of a randomized trial with an intensive low-fat dietary intervention.

A 5.5-fold range in breast cancer incidence rates in 21 countries shows strong correlation with national estimates of per capita intake of dietary fat, but not with other caloric sources (proteins and carbohydrates). It is argued that certain breast cancer and hormone factors may contribute little to the explanation of such international variations in incidence of this neoplasm. It is further argued that experimental studies in animals support a specific role for dietary fat in the promotion of mammary tumors, but the effects of calories alone seem to be largely restricted to tumor initiation. Finally, data from international, migrant-population, and analytic epidemiologic investigations are used to motivate the basic relative risk assumption of study designs thus far proposed for the Women's Health Trial, and some continuing motivations for a dietary intervention (low-fat diet) trial are discussed.

The biologic relation between dietary fats and serum cholesterol established in controlled dietary studies usually has not been found in cross-sectional studies of the general population. In vegetarian groups, dietary variables and serum cholesterol have been correlated significantly. To examine the role of technique of dietary assessment versus the dietary pattern of vegetarians, the authors studied the relation of diet with total serum cholesterol in 46 predominantly vegetarian adults in the Boston, Massachusetts, area in 1973-1974. The basis of the dietary information was 10-day diet records. Total serum cholesterol was positively associated with dietary cholesterol (r = 0.53) and saturated fatty acids (r = 0.50) in partial correlation analysis adjusted for age, sex, and triceps skinfold. The use of one-day dietary records lowered these correlation coefficients to about 0.3. Analysis of the components of variation of nutrient intake demonstrated that the vegetarians had a lower within-person variance, a higher between-person variance, or both compared with nonvegetarian study groups. Biologic responsiveness to dietary fat in the vegetarians was similar to that predicted by the Keys equation derived from nonvegetarians. Therefore, multiple-day averaging of dietary records and relatively smaller ratio of within-person to between-person variation in intake favor the detection of cross-sectional associations of diet with serum cholesterol.