The association of dietary fat and plant foods with endometrial cancer (United States)

Objectives: To examine the associations of dietary fat and selected plant foods with endometrial cancer in a population-based case–control study. Methods: Six hundred and seventy-nine incident cases of endometrial cancer diagnosed between 1985 and 1991, and 944 population-based controls completed a 98-item semi-quantitative food-frequency questionnaire and a detailed in-person interview which collected information on endometrial cancer risk factors. Logistic regression was used to estimate odds ratios (OR) and their 95% confidence intervals (CI) of endometrial cancer, adjusted for age, county, energy intake, hormone use, smoking and, in separate models, for body mass index (BMI: kg/m²). Results: Percent energy from fat was associated with an increased risk of endometrial cancer (highest quintile cf. lowest: OR = 1.8, 95% CI 1.3–2.6), with saturated and monounsaturated fats being the main contributors of risk. There was a stronger association between dietary fat and endometrial cancer among groups with higher circulating estrogen levels (i.e. women with higher BMI, users of unopposed estrogens, non-smokers, and younger age at menarche). Consumption of fruits or vegetables was inversely associated with endometrial cancer risk (highest quintile cf. lowest: OR = 0.65, 95% CI 0.46–0.93 and OR = 0.61, 95% CI 0.43–0.88, respectively). Further adjustment for BMI resulted in little or no attenuation of the ORs and associated CIs. Conclusions: These results provide support for the theory that a low-fat, high-fruit and high-vegetable diet may reduce the risk of endometrial cancer, and that these dietary factors may act independently of the effect of BMI.     

Dramatic dietary fat reduction is feasible for breast cancer patients: Results of the randomised study, WINS (UK) – Stage 1

Introduction

The influence of dietary fat on breast tumour growth¹ and, more recently, on treatment outcomes, ^{[2] and [3]} suggests an important role for dietary advice in the future health of breast cancer patients. The Women’s Intervention Nutrition Study (UK) – Stage 1 assessed the feasibility of achieving and maintaining a ≥50% reduction in reported fat intake in postmenopausal, early stage breast cancer patients in the UK.

Method

This study recruited patients in South-east England between 2000 and 2005. They were randomly allocated into two groups. Group 1 (n = 54), received specific dietary counselling to halve their reported fat intake and maintain this low fat intake. Group 2 (n = 53) received healthy eating advice only. Dietitian-led group sessions provided support for women in both groups over 2 years.⁴ Validated four-day diaries were used to measure intake. Data analysis used Generalised Linear Model (GLM) for repeated measures and logistic regression.

Results

A significantly greater proportion of women in Group 1 reported a fat intake reduction of ≥50% at 3 months (p < .001) and 24 months (p < .001) than in Group 2. The size of the effect of active dietary counselling was 37% at 3 months (95%CI: 21–54%) and 35% at 24 months (95%CI: 17–53%). Mean fat intake was halved at 3 months and 24 months in Group 1 only.

Conclusion

Demonstrating such feasibility is a key step towards defining diet’s role in the secondary prevention of breast cancer.     

Association of dietary fat intakes with risk of esophageal and gastric cancer in the NIH-AARP diet and health study

The aim of our study was to investigate whether intakes of total fat and fat subtypes were associated with esophageal adenocarcinoma (EAC), esophageal squamous cell carcinoma (ESCC), gastric cardia or gastric noncardia adenocarcinoma. From 1995-1996, dietary intake data was reported by 494,978 participants of the NIH-AARP cohort. The 630 EAC, 215 ESCC, 454 gastric cardia and 501 gastric noncardia adenocarcinomas accrued to the cohort. Cox proportional hazards regression was used to examine the association between the dietary fat intakes, whilst adjusting for potential confounders. Although apparent associations were observed in energy-adjusted models, multivariate adjustment attenuated results to null [e.g., EAC energy adjusted hazard ratio (HR) and 95% confidence interval (95% CI) 1.66 (1.27-2.18) p for trend <0.01; EAC multivariate adjusted HR (95% CI) 1.17 (0.84-1.64) p for trend = 0.58]. Similar patterns were also observed for fat subtypes [e.g., EAC saturated fat, energy adjusted HR (95% CI) 1.79 (1.37-2.33) p for trend <0.01; EAC saturated fat, multivariate adjusted HR (95% CI) 1.27 (0.91-1.78) p for trend = 0.28]. However, in multivariate models an inverse association for polyunsaturated fat (continuous) was seen for EAC in subjects with a body mass index (BMI) in the normal range (18.5-<25 kg/m(2)) [HR (95% CI) 0.76 (0.63-0.92)], that was not present in overweight subjects [HR (95% CI) 1.04 (0.96-1.14)], or in unstratified analysis [HR (95% CI) 0.97 (0.90-1.05)]. p for interaction = 0.02. Overall, we found null associations between the dietary fat intakes with esophageal or gastric cancer risk; although a protective effect of polyunsaturated fat intake was seen for EAC in subjects with a normal BMI.     

Dietary fat and breast cancer risk in the Swedish women's lifestyle and health cohort

We investigated whether dietary intakes of total fat, monounsaturated fat (MUFA), polyunsaturated fat (PUFA) and saturated fat (SFA) were associated with breast cancer risk in a prospective cohort of 49 261 Swedish women (30-49 years at enrolment), which yielded 974 breast cancer cases by December 2005. Further, we evaluated if associations differed by oestrogen and/or progesterone receptor tumour status. Total fat, MUFA, PUFA or SFA were not associated with risk overall. However, women in the highest MUFA and PUFA quintile intake had a reduced breast cancer risk after age 50 years (hazard ratios: 95% confidence interval=0.45: 0.25-0.99 and 0.54: 0.35-0.85, respectively) compared to women in the lowest quintile. The associations did not differ by oestrogen or progesterone receptor status. Despite the negative findings, type of fat during premenopausal years may have later differential effects on risk.     

Olive oil,other dietary fats,and the risk of breast cancer (Italy)

Data from a multicenter case-control study on breast cancer conducted in Italy have been used to analyze the relationship of olive oil and other dietary fats to breast cancer risk. Cases were 2,564 women hospitalized with histologically confirmed, incident breast cancer. Controls were 2,588 women admitted to the same network of hospitals for acute, non-neoplastic, non-hormone related, on-digestive tract disorders. Cases and controls were interviewed between 1991 and 1994 using a validated food-frequency questionnaire. The data were modelled through multiple logistic regression controlling for demographic and reproductive breast-cancer risk factors, energy intake and, mutually, for types of dietary fat. For olive oil, compared with the lowest quintile, the odds ratios (OR) were 1.05, 0.99, 0.93, and 0.87 for increasing quintiles of intake; in a model postulating linear logit increase, the OR per unit (30g) was 0.89 (95 percent confidence interval [CI]=0.81–0.99, P=0.03). Among other oils or fats considered, the OR for the highest level of intake was 0.72 (CI=0.6–0.9) for a group of specific seed oils (including safflower, maize, peanut, and soya) compared with nonusers. The ORs for the highest cf lowest level of intake were 0.80 for mixed or unspecified seed oils, 0.95 for butter, and 0.96 for margarine. The study, based on a large dataset from various Italian regions, shows an inverse relationship of breast cancer risk with intake of olive oil and other vegetable oils, but not with butter or margarine.     

Consumption of animal products, olive oil and dietary fat and results from the Belgian case-control study on bladder cancer risk

Aim

The Western diet typically consists of high levels of saturated fat from animal products and has been associated with an increased risk of bladder cancer. Whilst olive oil, the predominant fat in the Mediterranean diet, has been associated with many health benefits its role in bladder cancer aetiology is still unknown. Therefore, we investigated the effect of intake of animal products, olive oil and other major dietary fats on bladder cancer risk.

Methods

Dietary data were collected from 200 cases and 386 controls participating in a Belgian case-control study on bladder cancer. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) by comparing the highest with the lowest tertiles of intake between cases and controls using unconditional logistic regression. Adjustment was made for age, sex, smoking characteristics, occupational exposures and calorie intake.

Results

There was a statistically significant inverse association between olive oil intake and bladder cancer consistent with a linear dose-response relationship: middle versus the lowest tertile (OR: 0.62; 95% CI: 0.39-0.99) and the highest versus the lowest tertile (OR: 0.47; 95% CI: 0.28-0.78; p-trend = 0.002). We also observed borderline statistically significant increased odds of bladder cancer for the highest versus the lowest intake of cheese (OR: 1.53; 95% CI: 0.95-2.46; p-trend = 0.08). No potential associations were detected for any other source or type of dietary fat.

Conclusion

We observed evidence for a protective effect by olive oil and a possible increased risk of bladder cancer associated with a high intake of cheese. Our results require further investigation and confirmation by other studies.     

Effect of a low-fat,high-carbohydrate dietary intervention on change in mammographic density over menopause

We have previously shown that a low-fat dietary intervention for 2 years in women with extensive mammographic density decreased mammographic density to a greater extent than in the control group. Post-hoc analysis indicated that this effect was strongest in women who became postmenopausal during the follow-up period. The purpose of the present study was to determine if this potentially important finding could be confirmed in a new and larger group of subjects with a longer follow-up time. Participants in a low-fat dietary intervention trial who were premenopausal at entry and became postmenopausal during follow-up were examined. Total breast, dense, and non-dense area and percent density were measured in baseline and postmenopause mammograms using a computer-assisted method. Total breast and non dense area increased more in the control group compared to the intervention group (for breast area 2.6 and 0.2 cm², respectively; P = 0.05, and for non-dense area 10.9 and 8.1 cm², respectively; P = 0.06). Dense area decreased to a similar degree in both groups (−8.2 and −8.0 cm², respectively; P = 0.84). Percent density decreased to a slightly greater degree in the control compared to intervention group (−9.4 and −7.8%, respectively, P = 0.11). There were no significant differences between study groups after adjustment for weight change. Menopause reduced density to a similar extent in the low-fat diet and control groups. If a low-fat diet reduces breast cancer risk, the effect is unlikely to be through changes in mammographic density at menopause.     

Dietary fat intake and liver cancer risk: A prospective cohort study in Chinese women

Objective:This study aimed to determine whether dietary fat intake increased liver cancer risk in Chinese women from a prospective population-based cohort.Methods:A total of 72,704 Chinese women were followed up from the time of baseline recruitment (1996–2000) to the end of 2016. Dietary fat intake was calculated using a validated food frequency questionnaire. The Cox regression model was used to assess the hazard ratio (HR) and 95% confidence intervals (CI) for dietary fat intake and liver cancer risk.Results:We identified 252 incident liver cancer cases out of 1,267,845 person-years during the overall follow-up time. Null associations, neither in quartiles nor per standard deviation (SD) increment, were detected between liver cancer risk and dietary total fat, fat subtypes and subtype ratios, and food sources. The HR (95% CI) of the 1-SD increment was 1.03 (0.90–1.17) for total fat, 1.06 (0.93–1.20) for saturated fat, 1.06 (0.93–1.21) for monounsaturated fat, and 1.00 (0.89–1.13) for polyunsaturated fat. Similar null associations were observed in stratification analyses according to body mass index and menopausal status.Conclusions:In our prospective cohort study, no significant association was observed in Chinese women between dietary fat and liver cancer risk, and in stratification and sensitivity analyses.     

Dietary fat and lung cancer: a case-control study in Uruguay

To examine whether dietary fat and cholesterol modifies lung cancer risk, a case-control study was conducted in Uruguay of 426 men diagnosed from1993 to 1996 with lung cancer, and 419 hospitalized frequency-matched controls. Dietary patterns were assessed using a 64-item food frequency questionnaire, which allowed the calculation of total energy intake. After adjustment for potential confounders through a model which included tobacco smoking, total energy, a term for all vegetables and fruits, and a-carotene in take, an increase in risk for total fat intake for all cell types of lung cancer was observed. Adenocarcinoma of the lung was associated strongly with saturated fat intake (odds ratio [OR] = 2.3, 95 percent confidence interval[CI] = 1.2-4.4), whereas small-cell lung cancer was associated with dietary cholesterol (OR = 2.8, CI = 1.1-7.5). These results suggest that the association of saturated fat and cholesterol could be type-specific, but the high correlation existing between dietary lipids precludes any strong statement about this point. This revised version was published online in July 2006 with corrections to the Cover Date.     

The relationship between dietary fat intake and risk of colorectal cancer: evidence from the combined analysis of 13 case-control studies

The objective of this study was to examine the effects of the intakeof dietary fat upon colorectal cancer risk in a combined analysis of datafrom 13 case-control studies previously conducted in populations withdiffering colorectal cancer rates and dietary practices. Original datarecords for 5,287 cases of colorectal cancer and 10,470 controls werecombined. Logistic regression analysis was used to estimate odds ratios (OR)for intakes of total energy, total fat and its components, and cholesterol.Positive associations with energy intake were observed for 11 of the 13studies. However, there was little, if any, evidence of anyenergy-independent effect of either total fat with ORs of 1.00, 0.95, 1.01,1.02, and 0.92 for quintiles of residuals of total fat intake (P trend =0.67) or for saturated fat with ORs of 1.00, 1.08, 1.06, 1.21, and 1.06 (Ptrend = 0.39). The analysis suggests that, among these case-control studies,there is no energy-independent association between dietary fat intake andrisk of colorectal cancer. It also suggests that simple substitution of fatby other sources of calories is unlikely to reduce meaningfully the risk ofcolorectal cancer.     

A study of diet and breast cancer prevention in Canada: why healthy women participate in controlled trials

Little research has been undertaken to determine why healthy people agree to enroll in randomized controlled trials of cancer prevention. This study describes the beliefs of Canadian women participating in a trial designed to determine the effect of reducing dietary fat on the development of breast cancer. Healthier eating, nutritional counseling, contributing to science, and helping others were the most frequently cited advantages of participation. Weight control and general better health were specifically associated with the dietary regimens. Attending appointments and difficulties when eating out were the main disadvantages of participation. Suggestions that would promote adherence to the trial protocol also were elicited. Responses cited most often included opportunities to meet other participants, more nutritional counseling (particularly psychological tips), updates about the trial, and more recipes. Attention should be paid to these suggestions as they characterize some of the major determinants of adherence behavior.Drs Till and Boyd, and Mss Sutherland, Martin, and Greenberg are with the Division of Epidemiology & Statistics, Ontario Cancer Institute/Princess Margaret Hospital, Toronto, Canada. Ms Carlin and Mr Harper were summer students in the Division. Address correspondence to Ms Sutherland, Division of Epidemiology and Statistics, Ontario Cancer Institute, 500 Sherbourne Street, Toronto, Canada, M4X 1K9. This research was supported by The National Cancer Institute of Canada with funds from the Canadian Cancer Society. Dr Boyd is the recipient of a National Health Scientist award from Health and Welfare, Canada.     

The effect of dietary fat on breast cancer survival among Caucasian and Japanese women in Hawaii

182 Japanese and 161 Caucasian breast cancer patients participated in an epidemiologic case-control study from 1975–1980. They were subsequently followed until the end of 1987 to determine their survival status. Among the Japanese, patients with regional or distant disease had a relative risk (RR) of death of 13.0 (95% Confidence Interval (CI), 4.3–39.1) compared to those within situ or localized disease, and obese patients had a RR of death of 3.5 (95% CI, 1.3–10.0) compared to non-obese subjects. Among the Caucasians, patients with advanced disease had a RR of death of 4.3 (95% CI, 1.8–10.5) compared to those within situ or localized disease, and patients with a high fat intake had a RR of 3.2 (95% CI, 1.2–8.6) compared to subjects with a low fat intake. Menopausal status (pre- or postmenopausal) and replacement estrogen use were not related to survival from breast cancer in either ethnic group. When Japanese and Caucasian patients were compared with each other, there was no significant difference in survival between them.     

Self-reported health and use of health care services in long-term cancer survivors

Owing to an increasing number of long-term cancer survivors, the use of health care services and somatic health problems were compared between cancer survivors and a noncancer population. Data from the Nord-Trondelag Health Survey 2 (HUNT 2, 1995-1997) was merged with the Cancer Registry of Norway. Six cancer subgroups were constructed with diagnosis 5 years prior HUNT 2: testicular cancer (n= 59), colorectal cancer (n= 175), prostate cancer (n= 87), breast cancer (n= 258), gynaecological cancer (n= 153) and lymphoma/leukaemia (n= 83). For each cancer survivor 3 matched noncancer controls were selected from the HUNT 2 survey. The prevalence of common health problems, use of health care services and unfavourably life style parameters were compared between the 2 groups. Cancer survivors used health care services and received social welfare benefits more often than the controls. There was an increased risk of perceiving poor health after a history of cancer. Common health problems and/or unfavourable life style parameters could not explain poor health or the increased use of health care services among cancer survivors. Further studies are needed to investigate the reasons for increased use of health care services and perceived poor health in cancer survivors.     

Dietary fat intake and risk of ovarian cancer in the NIH-AARP Diet and Health Study

Background:

Fat intake has been postulated to increase risk of ovarian cancer, but previous studies have reported inconsistent results.

Methods:

The NIH-AARP Diet and Health Study, a large prospective cohort, assessed diet using a food frequency questionnaire at baseline in 1995–1996. During an average of 9 years of follow-up, 695 ovarian cancer cases were ascertained through the state cancer registry database. The relative risks (RRs) and 95% confidence interval (CI) were estimated using a Cox proportional hazard model.

Results:

Women in the highest vs the lowest quintile of total fat intake had a 28% increased risk of ovarian cancer (RR_{Q5 vs Q1}=1.28, 95% CI: 1.01–1.63). Fat intake from animal sources (RR_{Q5 vs Q1}=1.30; 95% CI: 1.02–1.66), but not from plant sources, was positively associated with ovarian cancer risk. Saturated and monounsaturated fat intakes were not related to risk of ovarian cancer, but polyunsaturated fat intake showed a weak positive association. The association between total fat intake and ovarian cancer was stronger in women who were nulliparous or never used oral contraceptives.

Conclusion:

Fat intake, especially from animal sources, was related to an increased risk of ovarian cancer. The association may be modified by parity and oral contraceptive use, which warrants further investigation.     

Dietary fat and cancer: consistency of the epidemiologic data,and disease prevention that may follow from a practical reduction in fat consumption

International variations and national time trends in disease rates suggest major associations between dietary fat and several important cancers. In contrast, case-control and cohort studies of dietary fat in relation to the same cancers generally report weak associations, or have failed to detect any association with fat intake. This study was undertaken in an attempt to understand the apparent discrepancy between these observations. The results provide an insight into the magnitude of cancer risk reduction that may follow from a practical reduction in dietary fat.Regression analyses of international variations in cancer incidence rates were used to estimate relative risks (RR) as a function of fat intakes for both males and females. These analyses focused on cancers of the breast, colon, rectum, ovary, and endometrium in females, and colon, rectum, and prostate cancers in males.Ages 55–69 and 30–44 were considered in order to compare RR estimates between an older and younger age group, and between post- and pre-menopausal women. Corresponding RR estimates were also calculated, based on the regression of changes in disease rates from the mid-1960s to 1980 on changes in dietary fat, using data from several countries. A strong degree of consistency with the RR estimates from international comparisons was observed. The international regression analyses were also used to project changes in cancer rates among Japanese migrants to the United States. A high level of consistency with the observed disease-rate changes was noted. Similarly, the international data analyses were used to project RRs for the fat intake categories used in specific case-control and cohort studies, while acknowledging measurement error in individual dietary assessment. Although certain exceptions are noted, considerable consistency was found between the aggregate and analytic data results, leaving open the strong possibility that a practical reduction in dietary fat could result in a major reduction in the incidence of several prominent cancers in the United States and in other nations having high fat consumption.This work was supported by grants GM-24472 and CA-38526 from the US National Institutes of Health.The authors are in the Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle WA 98104, USA, to which reprint requests should be addressed.     

Effect of dietary fat on codon 12 and 13 Ha-ras gene mutations in 2-amino-1-methyl-6-phenylimidazo-[4,5-b]pyridine–induced rat mammary gland tumors

Activating mutations in and expression of the Ha-ras gene were examined in benign and malignant female Sprague-Dawley rat mammary gland tumors induced by the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and promoted by a diet high in polyunsaturated fat. Ha-ras mutations were detected in codons 12 and 13 by selective polymerase chain reaction amplification of mutated sequences and nucleotide sequencing. The percentage of Ha-ras mutations in carcinomas from PhIP-treated rats was significantly higher in rats on a low-fat diet than in rats on a high-fat diet (82% (nine of 11) vs 26% (seven of 27), respectively, P < 0.01). In addition, whereas 56% of the carcinomas with Ha-ras mutations from rats on a low-fat diet carried double Ha-ras mutations, none of the carcinomas from rats on a high-fat diet had double mutations. Ha-ras mutations were also detected in benign tumors (largely adenomas) induced by PhIP in rats on different diets; two of eight and three of four benign tumors examined from rats on low-fat and high-fat diets, respectively, had Ha-ras mutations, suggesting that activating Ha-ras mutations alone are not sufficient for PhIP-induced tumors to become malignant. No differences were observed in the level of Ha-ras mRNA expression in the different groups. In our animal model, a high-fat diet increased the incidence and percentage of malignant PhIP-induced mammary gland tumors yet decreased the percentage of carcinomas showing Ha-ras mutations. Thus, the complement of genetic alterations associated with PhIP-induced mammary gland carcinogenesis is probably altered by the level of dietary fat. Mol. Carcinog. 20:348–354, 1997. © 1997 Wiley-Liss, Inc.     

Dietary carotenoids,vegetables, and lung cancer risk in women: the Missouri women's health study (United States)

Objective: To examine the effect of specific dietary carotenoids and their primary plant food sources on lung cancer risk in a population-based case–control study of women. Methods: Data were available for 587 incident primary lung cancer cases and 624 controls frequency matched to cases based on age. A modified version of the 100-item NCI-Block food-frequency questionnaire was used to obtain information concerning usual diet 2–3 years prior to interview. Results: In models adjusted for age, total calorie intake, pack-years of smoking, and education, -carotene, -cryptoxanthin, lutein + zeaxanthin, and total carotenoid intake were each associated with a significantly lower risk of lung cancer. Several vegetable groups were predictive of lower lung cancer risk, particularly the frequency of total vegetable intake. Individual and total carotenoids were no longer significantly associated with lower lung cancer risk in models adjusted for total vegetable intake. However, total vegetable intake remained significantly inversely associated with risk in models adjusted for total carotenoids. Conclusions: These results indicate that consumption of a wide variety of vegetables has a greater bearing on lung cancer risk in a population of smoking and nonsmoking women than intake of any specific carotenoid or total carotenoids.     

A cohort study of dietary carotenoids and lung cancer risk in women (Canada)

Objective: To investigate the association between dietary carotenoid intake and lung cancer risk in women. Methods: A case–cohort study was undertaken in the Canadian National Breast Screening Study dietary cohort, which consists of 56,837 women who completed a self-administered dietary questionnaire. The cohort was recruited between 1980 and 1985, and during follow-up to the end of 1993 a total of 196 cohort members were diagnosed with incident lung cancer. For analysis, a subcohort consisting of a random sample of 5681 women was selected from the full dietary cohort. After exclusions for various reasons, the analyses were based on 155 cases and 5361 non-cases. Results: When compared to those in the lowest quartile level of intake, the adjusted incidence rate ratios (95% confidence intervals) for those in the highest quartile levels of -carotene, -carotene, -cryptoxanthin, lycopene, and lutein intake were 0.90 (0.51–1.58), 1.40 (0.76–2.59), 0.66 (0.33–1.32), 1.04 (0.61–1.76), and 1.26 (0.70–2.24), respectively; none of the associated tests for trend was statistically significant. Conclusion: These results suggest that there is no association between dietary carotenoid intake and lung cancer risk, at least for the range of intakes observed here.     

The effects of a low-fat dietary intervention and tamoxifen adjuvant therapy on the serum estrogen and sex hormone-binding globulin concentrations of postmenopausal breast cancer patients

Summary The purpose of the study was to determine the effect of a low-fat dietary intervention, with or without concomitant tamoxifen adjuvant therapy, on serum estrogen and sex hormone-binding globulin (SHBG) levels in postmenopausal patients with resected breast cancer. Ninety-three patients were randomized to either reduce their fat intake to 15–20% of total calories, or to a dietary control group. Serum estradiol, estrone, estrone sulfate, and SHBG concentrations were assayed at baseline, and at 6, 12, and 18 months thereafter. In 19% of patients, the preintervention serum estradiol levels were below the sensitivity of the assay (5 pg/ml). Tamoxifen had no significant effect on serum estrogen levels, but produced an elevation in SHBG. Patients with reliably quantifiable preintervention estradiol concentrations ( 10 pg/ml) showed a significant reduction in serum estradiol after 6 months on the low-fat diet (average, 20%; p < 0.005); this was sustained over the 18 month study period. Serum SHBG levels were increased by tamoxifen therapy, but were reduced significantly (p = 0.01) after 12 months on the low-fat diet in patients not receiving tamoxifen. No changes in serum estrone or estrone sulfate resulted from the dietary intervention. While the low-fat diet produced significant weight loss, patients treated with tamoxifen without dietary intervention showed a gain in body weight. These weight changes produced disruptions in the normal positive correlation between body weight and serum estrone sulfate, and the negative correlation with SHBG concentration.     

Adult dietary intake and prostate cancer risk in Utah: a case-control study with special emphasis on aggressive tumors

A population-based case-control study in Utah of 358 cases diagnosed with prostate cancer between 1984 and 1985, and 679 controls categorically matched by age and county of residence, were interviewed to investigate the association between dietary intake of energy (kcal), fat, protein, vitamin A, beta-carotene, vitamin C, zinc, cadmium, selenium, and prostate cancer. Dietary data were ascertained using a quantitative food-frequency questionnaire. Data were analyzed separately by age (45-67, 68-74) and by tumor aggressiveness. The most significant associations were seen for older males and aggressive tumors. Dietary fat was the strongest risk factor for these males, with an odds ratio (OR) of 2.9 (95 percent confidence interval [CI] 1.0-8.4) for total fat; OR = 2.2 (CI = 0.7-6.6) for saturated fat; OR = 3.6 (CI = 1.3-9.7) for monounsaturated fat; and OR = 2.7 (CI = 1.1-6.8) for polyunsaturated fat. Protein and carbohydrates had positive but nonsignificant associations. Energy intake had an OR of 2.5 (CI = 1.0-6.5). In these older men, no effects were seen for dietary cholesterol, body mass, or physical activity. There was little association between prostate cancer and dietary intake of zinc, cadmium, selenium, vitamin C, and beta-carotene. Total vitamin A had a slight positive association with all prostate cancer (OR = 1.6, CI = 0.9-2.4), but not with aggressive tumors. No associations were found in younger males, with the exception of physical activity which showed active males to be at an increased but nonsignificant risk for aggressive tumors (OR = 2.0, CI = 0.8-5.2) and beta-carotene which showed a nonsignificant protective effect (OR = 0.6, CI = 0.3-1.6). The findings suggest that dietary intake, especially fats, may increase risk of aggressive prostate tumors in older males.