==================================CMR52================================== 52. Relationships between dietary fat and breast cancer. Qualitative effects of dietary lipids and breast cancer. Unsaturated vs. saturated fats. Including epidemiological studies, clinical trials, and animal models. 1 UI - 87092476 AU - Pariza MW TI - Calorie restriction, ad libitum feeding, and cancer. AB - The inhibition of cancer by calorie restriction was discovered over 50 years ago. By 1950 it had been well characterized and there existed sufficient data to propose a mechanism of action. For reasons that remain unclear, but are probably related to the perception of the calorie restricted rodent as "small: and the ad libitum feeding regimen as more "normal,: the concept of calorie restriction has been largely ignored by investigators after this time. Hence, despite the fact that calorie restriction is one of the oldest, best-documented, and most effective ways known to reduce cancer risk in rodents, it has had little impact on modern cancer research. In this report the history of calorie restriction is briefly reviewed, and a mechanism of action is proposed that involves increased production of ACTH and decreased production of gonadotrophins. It is further proposed that these changes may come about in part from the restriction of the time during which feeding is permitted as well as from the restriction of food per se. There is renewed interest in calorie restriction due in part to the growing recognition that there are differences in the efficiency of utilization of various sources of energy, in particular that fat calories are utilized more efficiently and provide more usable energy than carbohydrate calories. New data are presented indicating that the apparent enhancement by dietary fat of mammary cancer in rats is really a manifestation of the caloric effect. Further, the effect is abolished by moderate calorie restriction of only 15-20%. The application of these findings to the prevention of cancer in humans is considered. MH - Adrenocorticotropic Hormone/BIOSYNTHESIS ; Animal ; Body Weight ; Caloric Intake ; Dietary Carbohydrates/METABOLISM ; Dietary Fats/ METABOLISM ; *Eating ; Energy Metabolism ; *Food Deprivation ; Mammary Neoplasms, Experimental/ETIOLOGY/METABOLISM ; Neoplasms, Experimental/ETIOLOGY/*PREVENTION & CONTROL ; Review ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S. Gov't, P.H.S. SO - Proc Soc Exp Biol Med 1986 Dec;183(3):293-8 2 UI - 87085852 AU - Clinton SK ; Alster JM ; Imrey PB ; Nandkumar S ; Truex CR ; Visek WJ TI - Effects of dietary protein, fat and energy intake during an initiation phase study of 7,12-dimethylbenz[a]anthracene-induced breast cancer in rats. AB - A factorial experiment was conducted to examine the effects of dietary protein (8, 16, 32% of energy from casein) and dietary fat (12, 24, 48% of energy from corn oil) on the initiation of 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast carcinogenesis in rats. Forty weanling female Sprague-Dawley rats were assigned to each of nine diets fed ad libitum. After 4 wk each rat received DMBA (20 mg/kg) via gastric intubation. For an additional 22 wk after carcinogen administration all rats consumed a diet containing 16% of dietary energy from protein and 24% from fat. Dietary fat, protein and ad libitum energy consumption exhibited statistically significant effects on final tumor prevalence, but interactive effects were not found. At necropsy, rats fed corn oil at 12, 24 and 48% of energy prior to DMBA administration showed tumor prevalences of 58, 58 and 85% with 116, 153 and 231 total tumors, respectively. The data indicate a significant nonlinear effect of dietary fat. Corresponding numbers for rats fed casein at 8, 16 and 32% of energy prior to DMBA were prevalences of 79, 65 and 59%, with total tumor counts of 194, 144 and 162. Higher dietary protein during the initiation phase was associated with a significant reduction in tumor prevalence, which was most striking between 8 and 16% of energy from protein. In addition, results of multiple logistic regression showed that tumorigenesis was increased with greater ad libitum energy intake. The odds of a tumor at necropsy were multiplied by 1.19 for each kilocalorie increase in ad libitum energy intake averaged over the post-DMBA phase of the experiment. An additional six weanling rats fed each diet for 4 wk were killed for assay of hepatic carcinogen metabolizing enzymes at the time corresponding to DMBA administration in the initiation experiment. Both protein and fat showed independent effects on the activity of several enzymes. However, enzyme activity did not suggest a unifying mechanism whereby these nutrients influence DMBA-induced mammary carcinogenesis. MH - Adenocarcinoma/ETIOLOGY ; Adenoma/ETIOLOGY ; Animal ; *Caloric Intake ; Carcinogens/METABOLISM ; Dietary Fats/*ADMINISTRATION & DOSAGE/PHARMACODYNAMICS ; Dietary Proteins/*ADMINISTRATION & DOSAGE/PHARMACODYNAMICS ; Female ; Mammary Neoplasms, Experimental/*ETIOLOGY/PREVENTION & CONTROL ; Microsomes, Liver/ DRUG EFFECTS/ENZYMOLOGY ; Rats ; Rats, Inbred Strains ; Support, U.S. Gov't, P.H.S. ; *9,10-Dimethyl-1,2-Benzanthracene SO - J Nutr 1986 Nov;116(11):2290-302 3 UI - 87067576 AU - Hawrylewicz EJ TI - Fat-protein interaction, defined 2-generation studies. AB - Mammary tumor burden, in rats fed either normal or high fat diets related positively to the level of protein in the diet. This relationship existed with either a direct (NMU) or indirect carcinogen (DMBA). Significant differences in body growth, sexual maturation, morphologic structures in the mammary duct, and hormone activities during the estrous cycle probably contributed to lower tumor burden in the low protein-normal fat (LP-NF) group. Animals fed a high protein-normal fat (HP-NF) diet throughout their entire life have, with the exception of early sexual maturation, no distinctive characteristics compared to the control group. Inspite of these physical and physiologic similarities, increased dietary protein enhanced the effect of administered carcinogens. Animals fed a high protein-high fat (HP-HF) diet were compared to rats fed a normal protein-high fat (NP-HF) diet. Increased dietary protein further enhanced the effect of the high fat diet resulting in an increased carcinogen-induced tumor burden. These studies indicate that the design of the animal model, i.e. age of initiation of a test diet, appears to have a significant bearing on mammary tumor development. The biologic mechanisms which respond to diet modifications and which may influence breast tumor growth have not been thoroughly elaborated and require additional study. MH - Animal ; Body Weight ; Cell Transformation, Neoplastic/DRUG EFFECTS ; Cocarcinogenesis ; Dietary Fats/ADMINISTRATION & DOSAGE/ *METABOLISM ; Dietary Proteins/ADMINISTRATION & DOSAGE/ *METABOLISM ; Disease Models, Animal ; Eating ; Epidemiologic Methods ; Mammae/DRUG EFFECTS ; Mammary Neoplasms, Experimental/ ETIOLOGY ; Methylnitrosourea ; Prolactin/BLOOD ; Review ; Thymidine/METABOLISM ; 9,10-Dimethyl-1,2-Benzanthracene SO - Prog Clin Biol Res 1986;222:403-33 4 UI - 87030455 AU - Elegbede JA ; Elson CE ; Qureshi A ; Dennis WH ; Yatvin MB TI - Increasing the thermosensitivity of a mammary tumor (CA755) through dietary modification. AB - Disruption of the integrity of tumor cellular membranes has been proposed as an initiating event in hyperthermic cell death. Thermosensitivity measured by the shift in the harmonic mean of tumor regrowth delay of CA755 mammary adenocarcinomas grown in the hind legs of male BDF1, mice increased 22% when the hosts were fed a diet enriched in polyunsaturated fatty acids. Although the diet elicited the anticipated increase in tumor membrane phospholipid polyunsaturated fatty acids, the proportion of total unsaturated fatty acids decreased and the proportion of membrane-rigidifying saturated fatty acids increased. Concomitantly, the concentrations of cholesterol and phospholipid phosphorus increased and the ratio of phosphatidylethanolamine to phosphatidylcholine decreased, presumably to counter the effect of the change in the fatty acid pattern. In host liver membranes, the diet-mediated increase in proportion of polyunsaturated fatty acids was not accompanied by an increase in the proportion of rigidifying saturated fatty acids. Instead, the homeoviscous adaptation consisted of decreases in monounsaturated fatty acids and cholesterol concentration and an increase in the phosphatidylethanolamine-phosphatidylcholine ratio. Addition of a natural inhibitor of cholesterol biosynthesis to the polyunsaturated fatty acid enriched-diet reversed the diet-mediated increase in the phosphatidylethanolamine-phosphatidylcholine ratio of host liver membranes. Tumor membrane lipids from hosts fed the combined dietary factors were characterized by the formentioned rigidifying increase in saturated fatty acids and compensatory decrease in the phosphatidylethanolamine-phosphatidylcholine ratio. The inhibitor reversed the compensatory increases in cholesterol and phospholipid phosphorus concentrations. As a consequence the thermosensitivity of tumors bearing this perturbed membrane was increased. MH - Adenocarcinoma/PHYSIOPATHOLOGY ; Animal ; Anticholesteremic Agents/PHARMACODYNAMICS ; Body Weight ; Cell Survival ; Cholesterol/BLOOD ; *Dietary Fats ; Fatty Acids, Unsaturated ; *Heat ; Liver/PATHOLOGY ; Mammary Neoplasms, Experimental/ METABOLISM/*PHYSIOPATHOLOGY ; Membrane Lipids/METABOLISM ; Mice ; Mice, Inbred Strains ; Organ Weight ; Phospholipids/METABOLISM ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Eur J Cancer Clin Oncol 1986 May;22(5):607-15 5 UI - 87027938 AU - Rose DP ; Boyar AP ; Wynder EL TI - International comparisons of mortality rates for cancer of the breast, ovary, prostate, and colon, and per capita food consumption. AB - The 1978-1979 mortality rates for cancers of the breast, prostate, ovary, and colon in 26 to 30 countries were related to the average 1979-1981 food availability data published by the United Nations. The previously described relationship between breast cancer mortality rates and animal fat consumption continues to be evident, and applies also to the other three tumor types. The correlation with breast cancer was particularly strong in postmenopausal women. Since 1964, particularly notable increases in both breast cancer mortality rate and dietary fat intake have occurred in those countries with a relatively low breast cancer risk. The international comparisons support evidence from animal experiments that diets in which olive oil is a major source of fat are associated with reduced breast cancer risk. The excess in mortality rates for breast and ovarian cancer in Israel relative to the national animal fat consumption may be due to the mixed ethnic origin of the Israeli population. Positive correlations between foods and cancer mortality rates were particularly strong in the case of meats and milk for breast cancer, milk for prostate and ovarian cancer, and meats for colon cancer. All four tumor types showed a negative correlation with cereal intake, which was particularly strong in the case of prostate and ovarian cancer. Although, in general, there was a good positive correlation between prostate and breast cancer mortality rates and between prostate cancer and animal fat, discrepancies in national ranking indicate the operation of other etiologic factors that modify risk. The observed positive correlations between the four cancer mortality rates and caloric intake from animal sources, but negative correlations for vegetable-derived calories, suggest that, of the two, animal fat and not energy is the major dietary influence on cancer risk. MH - Adult ; Breast Neoplasms/*MORTALITY ; Caloric Intake ; Colonic Neoplasms/*MORTALITY ; Comparative Study ; *Diet ; Dietary Fats ; Female ; Human ; Male ; Menopause ; Middle Age ; Ovarian Neoplasms/*MORTALITY ; Plant Oils ; Prostatic Neoplasms/ *MORTALITY ; Support, U.S. Gov't, P.H.S. ; World Health SO - Cancer 1986 Dec 1;58(11):2363-71 6 UI - 87004446 AU - Pariza MW ; Hargraves WA ; Benjamin H ; Christou M ; Jefcoate CR ; Storkson J ; Albright K ; Kraus D ; Sharp P ; Boissonneault GA ; et al TI - Modulation of carcinogenesis by dietary factors. AB - The purpose of this report is to present recent data on two modulating factors of carcinogenesis that are found in Western-type diets: a beef-derived mutagenesis modulator that has been shown to inhibit the initiation of epidermal carcinogenesis in mice, and the possible role of net energy rather than dietary fat per se in the enhancement of rat mammary carcinogenesis. MH - Animal ; *Carcinogens ; Cattle ; *Diet/ADVERSE EFFECTS ; Dietary Fats/ADVERSE EFFECTS ; Energy Metabolism ; Female ; Mammary Neoplasms, Experimental/ETIOLOGY ; Meat ; Mice ; Mutation ; Rats ; Rats, Inbred F344 ; Skin Neoplasms/PREVENTION & CONTROL ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S. Gov't, P.H.S. SO - Environ Health Perspect 1986 Aug;67:25-9 7 UI - 87001945 AU - Wynder EL ; Rose DP ; Cohen LA TI - Diet and breast cancer in causation and therapy. AB - The major macronutrient associated with increased breast cancer risk is dietary fat. Evidence for this association is based on epidemiologic, clinical, and laboratory animal studies. In addition, there is suggestive epidemiologic evidence that differences in postmastectomy survival rates in Japan and the United States may be attributable to differences in dietary fat intake. The importance of the type of fat consumed, as well as its amount, has emerged as an issue of major importance. Some oils, including those rich in monounsaturates, medium chain fatty acids, or omega-3 (n-3) fatty acids appear to lack tumor-promoting effects despite their presence in the diet at high levels. Possible mechanisms by which dietary fat may exert its effects could be either direct or indirect. Direct mechanisms involve dietary modification of membrane structure and function; indirect mechanisms involve alterations in the endocrine system, and/or the metabolism of essential fatty acids to biologically active eicosanoids such as prostaglandins, and suppression of immune responses. Dietary guidelines and dietary intervention trials for the primary and secondary prevention of breast cancer are discussed. MH - Animal ; Breast Neoplasms/BLOOD/*ETIOLOGY/OCCURRENCE ; Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ; Female ; Hormones/BLOOD ; Human ; Japan ; Male ; Mammary Neoplasms, Experimental/ETIOLOGY ; Mice ; Prostatic Neoplasms/ETIOLOGY/ OCCURRENCE ; Rats ; Support, U.S. Gov't, P.H.S. ; United States SO - Cancer 1986 Oct 15;58(8 Suppl):1804-13 8 UI - 86229821 AU - Rogers AE ; Conner B ; Boulanger C ; Lee S TI - Mammary tumorigenesis in rats fed diets high in lard. AB - Studies were performed to examine the effect of a lard diet on tumorigenesis by 7,12-dimethylbenzanthracene (DMBA), given parenterally rather than by gavage, to eliminate any effect of the high lard diet on carcinogen absorption. In addition, the effect of low dietary levels of the antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in the tumor model was evaluated. The lards fed were analyzed for fatty acid composition and content of certain potential contaminants. DMBA induced tumors when given by intravenous or subcutaneous injection. The high lard diet appeared to enhance tumorigenesis in rats given a dose of 0.25 mg (10% of the gavage dose) by injection into the mammary gland, although the effect was not statistically significant. In other experiments using lard from different sources and DMBA given by gavage, significant enhancement of tumorigenesis was limited to groups fed the high lard diets throughout the experiment or beginning after DMBA exposure. In contrast to earlier results, there was no demonstrable effect of feeding the high lard diets before DMBA administration. Addition of BHA and BHT to the lard at the concentration assayed in commercial lard samples or at the maximum concentration permitted did not influence the tumorigenesis. In groups in which tumorigenesis was enhanced by the high lard diet, the incidence of malignant, invasive tumors was higher than in other groups. MH - Animal ; Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ; Female ; Mammary Neoplasms, Experimental/ETIOLOGY/*PATHOLOGY ; Rats ; Rats, Inbred Strains ; Support, U.S. Gov't, P.H.S. ; Time Factors ; 9,10-Dimethyl-1,2-Benzanthracene SO - Lipids 1986 Apr;21(4):275-80 9 UI - 86228507 AU - Gabor H ; Abraham S TI - Effect of dietary menhaden oil on tumor cell loss and the accumulation of mass of a transplantable mammary adenocarcinoma in BALB/c mice. AB - A reduction in the size of transplantable mammary adenocarcinoma IX was achieved when female BALB/c mice were fed isocaloric 10% fat diets containing either hydrogenated cottonseed oil (HCTO) or menhaden oil (MO) as opposed to those mice fed corn oil (CO). Indeed, CO increased the size of the neoplasms when fed alone at 5 or 1% of the diet, although such diets contained less fat calories than did the 10% fat diets containing the other two oils. At the 10% level of dietary fat, enhanced accumulation of tumor mass was observed even when 7.5, 5.0, and 2.5% CO was administered in combination with either HCTO or MO. Although this effect of CO could not be inhibited when nine times as much HCTO was added to the diet, such growth enhancement was abolished when the diet contained nine times as much MO. Hence these experiments emphasized the importance of the type rather than the amount of dietary fat. Whereas MO contained polyunsaturated fatty acids (PUFA's) [approximately 1% as linoleic acid, approximately 16% as 5,8,11,14,17-eicosapentaenoic acid (EPA), approximately 11% as 4,7,10,13,16,19-docosahexaenoic acid (DHA)], HCTO contained none and CO had about 60% of its constituent fatty acids in the form of linoleic acid. The rate of tumor cell loss, determined by the [125I]5-iodo-2'-deoxyuridine method, in the 10% MO-fed or the 10% HCTO-fed mice (54 or 45%, respectively) was more than twice that observed for tumors from the 10% CO-fed mice (22%). These observations were discussed in terms of the influence of the dietary PUFA linoleic acid [C 18:2 (No. of carbons:No. of double bonds), n-6], the PUFA EPA (C 20:5, n-3), and the PUFA DHA (C 22:6, n-3) on the size of mammary tumors and on the involvement of prostaglandins in this process. MH - Adenocarcinoma/METABOLISM/*PATHOLOGY ; Animal ; Body Weight ; Cottonseed Oil/PHARMACODYNAMICS ; Dietary Fats/*PHARMACODYNAMICS ; Fatty Acids/ANALYSIS ; Female ; Linoleic Acids/METABOLISM ; Mammary Neoplasms, Experimental/METABOLISM/*PATHOLOGY ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Oils/ *PHARMACODYNAMICS ; Prostaglandins/BIOSYNTHESIS ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - JNCI 1986 Jun;76(6):1223-9 10 UI - 86308830 AU - L:e MG ; Moulton LH ; Hill C ; Kramar A TI - Consumption of dairy produce and alcohol in a case-control study of breast cancer. AB - In a French case-control study of 1,010 breast cancer cases and 1,950 controls with nonmalignant diseases, the risk of breast cancer was found to be positively associated with frequency of cheese consumption and the level of fat in the milk consumed. A negative association was found between frequency of yogurt consumption and the risk of breast cancer. No association was found between the consumption of butter and the risk of breast cancer. The positive association between a daily consumption of alcohol and the risk of breast cancer previously reported was not altered when dairy produce consumption was taken into account. MH - Aged ; *Alcohol Drinking ; Breast Neoplasms/*ETIOLOGY ; Cheese/ ADVERSE EFFECTS ; Dairy Products/*ADVERSE EFFECTS ; Dietary Fats/ ADVERSE EFFECTS ; Female ; Human ; Lactobacillus Acidophilus ; Middle Age ; Risk ; Support, Non-U.S. Gov't SO - JNCI 1986 Sep;77(3):633-6 11 UI - 86308825 AU - Lubin F ; Wax Y ; Modan B TI - Role of fat, animal protein, and dietary fiber in breast cancer etiology: a case-control study. AB - A case-control study of 818 breast cancer (BC) patients and 2 matched control groups, surgical controls (SCs) and neighborhood controls (NCs), was undertaken in Israel between 1975 and 1978. The interview schedule included a detailed dietary history based on the frequency of consumption of 250 food items, which were grouped according to their principal nutrient component. The average frequency of consumption of each food item in each nutrient group was computed. Medical, demographic, hormonal, and parity histories were also obtained. Risks associated with fat, animal protein, and fiber consumption were evaluated. Two types of analysis were performed [in 2 age groups (less than 50 yr and greater than or equal to 50 yr)], using the conditional logistic method: evaluating the risk attributable to nutrition only and controlling for nondietary confounding factors as well. When no adjustment for nondietary confounding factors was made, the risk increased with fat intake in both age groups [one-tailed P-value for linear trend = .08 and .07 in age less than 50 and .01 and .10 for the greater than or equal to 50 age category for the BC case (BCC)-SC and BCC-NC comparisons, respectively]. Increased fiber intake decreased the risk in the younger age group (one-tailed P-value for linear trend = .06 and .07 for the BCC-SC and BCC-NC comparisons, respectively), while in the 50-or-over age category the trend was inconsistent. The risk associated with animal protein was much less clear. For women in the highest quartiles of fat and animal protein intake and the lowest quartiles of fiber intake, risk was about twice as high as that for women in the lowest quartiles of fat and animal protein intake and in the highest quartile of fiber intake (one-tailed P-value for linear trend = .04 and .08 for age less than 50 and .08 and .09 for the age category greater than or equal to 50 BCC-SC and BCC-NC comparisons, respectively). When hormonal and demographic confounding factors were controlled for, this pattern persisted but it remained significant for 1 control only. Power increased when cases were analyzed against both controls simultaneously (one-tailed P-value for linear trend = .10 for age less than 50 and .02 for age greater than or equal to 50). Thus a higher fat-animal protein and lower fiber diet is associated with increased cancer risk, but this relationship needs to be studied further. MH - Adult ; Age Factors ; Aged ; Breast Neoplasms/*ETIOLOGY ; Dietary Fats/*ADMINISTRATION & DOSAGE ; Dietary Fiber/*ADMINISTRATION & DOSAGE ; Dietary Proteins/*ADMINISTRATION & DOSAGE ; Female ; Human ; Middle Age ; Risk ; Support, U.S. Gov't, P.H.S. SO - JNCI 1986 Sep;77(3):605-12 12 UI - 86307146 AU - Horwitt MK TI - The promotion of vitamin E. AB - Investigations that have influenced the promotion of vitamin E supplementation are reviewed. The various forms of vitamin E found in foods and the composition of synthetic vitamin E in common use are described with note of a frequent error of identification made in reports of studies on vitamin E. Recent communications on the use of antioxidants to delay carcinogenesis in animals and in humans are discussed. The publicity given the reports of cancer prevention by antioxidants will probably increase self-supplementations. It is therefore necessary to understand the pharmacological limits of such supplementation with vitamin E. Daily supplementation of adults with about 200 mg of d-alpha-tocopherol equivalents per day has not been proven to be harmful, but the effects of ingestion of more than 800 mg a day have not been studied sufficiently. Special precautions should be taken in administering emulsified vitamin E preparations intravenously to premature infants. MH - Animal ; Antioxidants ; Breast Neoplasms/BLOOD ; Chemistry ; Dietary Fats/ADMINISTRATION & DOSAGE/ADVERSE EFFECTS ; Female ; Human ; Infant ; Infant, Premature ; Lipid Peroxides/METABOLISM ; Male ; Mammary Neoplasms, Experimental/ETIOLOGY/PREVENTION & CONTROL ; Neoplasms, Experimental/PREVENTION & CONTROL ; Nomenclature ; Nutrition ; Nutritional Requirements ; Review ; Support, Non-U.S. Gov't ; Vitamin E/ADMINISTRATION & DOSAGE/ ADVERSE EFFECTS/BLOOD/*PHYSIOLOGY/THERAPEUTIC USE ; Vitamin E Deficiency/DRUG THERAPY SO - J Nutr 1986 Jul;116(7):1371-7 13 UI - 86286734 AU - Boylan ES ; Cohen LA TI - The influence of dietary fat on mammary tumor metastasis in the rat. AB - Young, virgin female Fischer 344 rats bearing the 13762 transplantable mammary tumor were fed diets containing either 5% (low-fat group) or 23% (high-fat group) corn oil for five weeks before and six weeks after tumor implantation. Animals in the two diet groups gained weight at comparable rates throughout the experiment. There was no significant difference between the low-fat and high-fat groups with respect to average tumor diameter measured twice per week for six weeks. At the time of death (6 weeks after tumor implantation), the lungs of all rats in both diet groups contained some metastatic tumor deposits; the volume of the metastases in the lungs varied widely in both groups. Numbers of metastases to regional lymph nodes and kidneys appeared unaffected by the fat content of the diet. Thus, both growth of the 13762 mammary tumor itself and metastatic spread from the tumor were comparable whether the young rats were fed a high-fat or a low-fat diet. MH - Animal ; Comparative Study ; Dietary Fats/*ADMINISTRATION & DOSAGE ; Female ; Lung Neoplasms/PATHOLOGY/SECONDARY ; Mammary Neoplasms, Experimental/*PATHOLOGY ; *Neoplasm Metastasis ; Neoplasm Transplantation ; Oils/ADMINISTRATION & DOSAGE ; Rats ; Rats, Inbred F344 ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Nutr Cancer 1986;8(3):193-200 14 UI - 86271915 AU - Hislop TG ; Coldman AJ ; Elwood JM ; Brauer G ; Kan L TI - Childhood and recent eating patterns and risk of breast cancer. AB - A case-control study was done to examine the relationship between childhood and recent eating practices and risk of breast cancer. Eight hundred forty-six cases and 862 controls returned questionnaires indicating their menopausal status. In premenopausal women, breast cancer risk was increased with recent consumption of foods high in fat content (gravy, beef, pork) and reduced with foods low in fat content (fish); in postmenopausal women, risk was increased with pork consumption only. Regarding carotene sources, risk was reduced with carrot consumption in postmenopausal women only. Similar trends in risk were not found for childhood eating practices. Body weight influenced the breast cancer risk differently for pre- and postmenopausal women: Heavier weight in childhood and teens reduced the risk of premenopausal breast cancer, and heavier weight in adulthood increased the risk of postmenopausal breast cancer. We conclude that fat consumption is associated with breast cancer, especially in premenopausal women. MH - Adult ; Body Height ; Body Weight ; Breast Neoplasms/*ETIOLOGY ; Child ; *Diet ; Dietary Fats ; Female ; Human ; Menopause ; Middle Age ; Obesity/COMPLICATIONS ; Questionnaires ; Risk ; Support, Non-U.S. Gov't SO - Cancer Detect Prev 1986;9(1-2):47-58 15 UI - 86271709 AU - Hawrylewicz EJ ; Huang HH ; Liu JM TI - Dietary protein, enhancement of N-nitrosomethylurea-induced mammary carcinogenesis, and their effect on hormone regulation in rats. AB - The effect of supplemental dietary protein (casein) fed with high fat diets was investigated using the N-nitrosomethylurea-induced mammary tumor model. Isocaloric diets containing casein and corn oil at 19 and 15% (normal protein-high fat) or 33 and 15% (high protein-high fat) were fed ad libitum to Sprague-Dawley mother rats. Female offspring continued on the diet. Food consumption and growth curves were similar over the entire growth period. N-Nitrosomethylurea (50 mg/kg body weight) or saline was administered at 7 and 8 weeks of age via the tail vein. Dietary protein had no effect on serum prolactin or growth hormone throughout the estrous cycle: Prior to carcinogen administration, at 7 weeks old, proestrus at 5 p.m., serum prolactin was 231.6 +/- 141.0 (SE) ng/ml (12 rats) versus 292.2 +/- 141.0 (13 rats) for normal versus high protein diet groups, respectively. No difference was noted after carcinogen injection at 9, 13, 28, and 33 weeks of age. Similarly no effect was noted on serum growth hormone activity. Tumor latency was 7 weeks and incidence was 100% in normal protein (24 rats) and high protein (39 rats) groups 28 weeks after carcinogen treatment. The number of tumors per rat (4.38 +/- 0.37 versus 2.87 +/- 0.35, P less than 0.002) and average tumor weight (17.97 +/- 2.63 versus 9.94 +/- 2.92 g) were significantly greater in the high protein group. Study indicates that diet or carcinogen treatment did not alter hormone regulation during the estrous cycle. However, supplemental dietary protein increased the effect of high fat diets enhancing the mammary tumor burden. MH - Animal ; Body Weight ; Caloric Intake ; Dietary Fats/PHYSIOLOGY ; Dietary Proteins/*PHYSIOLOGY ; Estrus ; Female ; Mammary Neoplasms, Experimental/CHEMICALLY INDUCED/*ETIOLOGY ; Methylnitrosourea ; Methyltyrosines/PHARMACODYNAMICS ; Prolactin/ BLOOD ; Rats ; Somatotropin/BLOOD ; Support, U.S. Gov't, P.H.S. SO - Cancer Res 1986 Sep;46(9):4395-9 16 UI - 86264637 AU - Boeryd B ; Hallgren B TI - The incidence of spontaneous mammary carcinoma in C3H mice is influenced by dietary fat given from weaning and given to the mothers during gestation and lactation. AB - The influence of dietary fat given to breeding C3H female mice during gestation and lactation on the incidence of spontaneous mammary carcinoma in the female offspring was studied. EWOS' commercial diet (E-diet) for mice and two test diets, one containing 2% soy oil (S-diet) and the other 2% soy oil and 0.1% methoxy-substituted glycerol ethers (MGE-diet), instead of the animal fat in the E-diet, were used. The breeding females were given the S- or MGE-diet during gestation and lactation and the progeny the S- or E-diet from weaning. The incidence of mammary carcinoma was studied in the force-bred progeny. The results disclosed significant correlations between the diets of the progeny and the number of litters and between the number of litters and the incidence of breast carcinoma. The results also indicated a strong influence of the mother's diet on the incidence of mammary carcinoma in the female progeny. MH - Age Factors ; Animal ; Dietary Fats/*ADVERSE EFFECTS ; Female ; Fertility ; Lactation ; Mammary Neoplasms, Experimental/*ETIOLOGY ; Mice ; Parity ; Pregnancy ; Support, Non-U.S. Gov't SO - Acta Pathol Microbiol Immunol Scand [A] 1986 May;94(3):237-41 17 UI - 86255105 AU - Cohen LA ; Thompson DO ; Choi K ; Karmali RA ; Rose DP TI - Dietary fat and mammary cancer. II. Modulation of serum and tumor lipid composition and tumor prostaglandins by different dietary fats: association with tumor incidence patterns. AB - For investigation of the role of linoleic acid (LA) and its biologically significant metabolites in mammary tumor promotion by dietary fat, a detailed study of the fatty acid group composition of serum lipids, tumor neutral lipids, tumor phospholipids, and tumor prostaglandins (PG's) was conducted in female inbred F344 rats initiated with N-nitrosomethylurea (CAS: 684-93-5) and fed diets containing various types and amounts of fat. The oils, safflower [23%, high fat (HF); 5%, low fat], corn (23%, 5%), olive (23%, 5%), and coconut (23%) varied widely with respect to their LA content and their polyunsaturate:monounsaturate:saturate ratios (9:1:1, 4.6:2.6:1, 0.6:5.9:1, and 0.008:0.05:1, respectively, for safflower, corn, olive, and coconut oils). A modified hexane-based technique was used for extraction of serum and tumor lipids. Total tumor lipids ranged from a low of 5 to a high of 228 mg/g (wet wt) with no differences found among the 7 dietary groups. The phospholipid content of the tumors ranged from 27 to 47% of total tumor lipid, again with no differences seen among dietary groups. Total serum lipids varied from a low of 3.77 mg/ml (safflower oil, 23%) to a high of 6.11 mg/ml (coconut oil, 23%), and an overall inverse trend was observed between total serum lipids and tumor incidence for the 4 HF diet groups. Serum cholesterol levels were significantly depressed in the HF safflower oil and corn oil groups compared to those in all other dietary groups and, in general, varied inversely with respect to mammary tumor incidence. Serum and tumor neutral fatty acid profiles closely reflected those of the diet, while tumor phospholipids appeared more resistant to diet-induced changes. Olive oil-fed animals exhibited high levels of oleic acid in both serum and tumor lipids. The levels of the major metabolite of LA, arachidonic acid (AA), in tumor phospholipids were highly variable and did not equate with dietary or serum LA levels. A positive association was found among dietary LA, tumor PGE2, and mammary tumor incidence among the 4 HF groups; however, no association was found between tumor AA levels and either tumor PGE2 levels or mammary tumor incidence. The results of this study suggest that dietary LA may exert its effects on mammary tumor promotion by virtue of its role as a PG precursor; but the precise steps in this sequence and possible competitive interactions between essential fatty acids, monoenes, and saturates and the PG-synthesizing system remain to be determined. MH - Animal ; Cholesterol/BLOOD ; Cocarcinogenesis ; Comparative Study ; Dietary Fats/ADVERSE EFFECTS/*METABOLISM ; Fatty Acids/ METABOLISM ; Female ; Mammary Neoplasms, Experimental/ETIOLOGY/ *METABOLISM/PATHOLOGY ; Methylnitrosourea/TOXICITY ; Oils/ADVERSE EFFECTS/*METABOLISM ; Phospholipids/METABOLISM ; Prostaglandins/ *METABOLISM ; Prostaglandins E/METABOLISM ; Prostaglandins F/ METABOLISM ; Radioimmunoassay ; Rats ; Rats, Inbred F344 ; Support, U.S. Gov't, P.H.S. ; Triglycerides/BLOOD SO - JNCI 1986 Jul;77(1):43-51 18 UI - 86255104 AU - Cohen LA ; Thompson DO ; Maeura Y ; Choi K ; Blank ME ; Rose DP TI - Dietary fat and mammary cancer. I. Promoting effects of different dietary fats on N-nitrosomethylurea-induced rat mammary tumorigenesis. AB - The promoting effects of diets varying both in type and amount of fat on N-nitrosomethylurea [(NMU) CAS: 684-93-5]-induced mammary tumorigenesis were assessed in female inbred F344 rats. Two seed oils (safflower and corn) and two fruit oils (olive and coconut), varying widely in their diene, monoene, and saturated fatty acid ratios, were fed in the casein-based AIN-76A diets at 23% [high-fat (HF) diet] and 5% [low-fat (LF) diet] by weight, with the exception of coconut oil which was fed only at 23%. The predominant fatty acid in safflower and corn oils was linoleic acid (82 and 56%, respectively), while the predominant fatty acids in olive and coconut oils were oleic (79%) and myristic (54%), respectively. The test diets were fed beginning 2 days after administration of NMU and continued until termination of the experiment at 22 weeks post NMU administration. Analysis of tumor incidence, latency, and multiplicity data obtained from the 7 experimental groups indicated that animals fed the HF safflower and corn oil diets exhibited enhanced mammary tumor yields when compared to animals fed HF olive or coconut oil diets or their LF counterparts. Since weight gains and total caloric intake were similar in all 4 HF groups, the results of this study indicate that the tumor-promoting properties of HF diets are more of a function of differences in fatty acid composition than of fat content per se or of total caloric intake. MH - Animal ; Body Weight ; Cocarcinogenesis ; Dietary Fats/*ADVERSE EFFECTS/ANALYSIS ; Fatty Acids/ANALYSIS ; Female ; Mammary Neoplasms, Experimental/BLOOD/*ETIOLOGY/PATHOLOGY ; Methylnitrosourea/*TOXICITY ; Oils/*ADVERSE EFFECTS/ANALYSIS ; Rats ; Rats, Inbred F344 ; Statistics ; Support, U.S. Gov't, P.H.S. ; Time Factors SO - JNCI 1986 Jul;77(1):33-42 19 UI - 86229823 AU - Braden LM ; Carroll KK TI - Dietary polyunsaturated fat in relation to mammary carcinogenesis in rats. AB - High fat diets promote the development of mammary tumors induced in rats by 7,12-dimethylbenz(a)anthracene (DMBA), and polyunsaturated fats are more effective than saturated fats. This difference is related to the linoleic acid content of polyunsaturated vegetable oils, but the amount of linoleate required for maximum tumor promotion appears to be higher than indicated by earlier experiments. Comparison of the effects of a polyunsaturated vegetable oil (corn oil) containing linoleate with a fish oil (menhaden oil) containing polyunsaturated fatty acids derived from linolenic acid showed that higher dietary levels of corn oil increased the yield of DMBA-induced mammary tumors, while corresponding levels of menhaden oil had an inhibitory effect. This is further evidence that promotion of mammary tumorigenesis by polyunsaturated vegetable oils may be mediated by prostaglandins or other biologically active eicosanoids derived from n-6 fatty acids. MH - Animal ; Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ; Fatty Acids/ANALYSIS ; Fatty Acids, Unsaturated/*ADVERSE EFFECTS ; Female ; Mammary Neoplasms, Experimental/*PATHOLOGY ; Oils/ ADVERSE EFFECTS ; Rats ; Rats, Inbred Strains ; Support, Non-U.S. Gov't ; 9,10-Dimethyl-1,2-Benzanthracene SO - Lipids 1986 Apr;21(4):285-8 20 UI - 86229820 AU - Kritchevsky D ; Weber MM ; Buck CL ; Klurfeld DM TI - Calories, fat and cancer. AB - The experiments reported are part of our effort to dissociate the tumor-enhancing effects of dietary fat and high caloric intake. Rats either were fed ad libitum diets containing 4% corn oil or their calories were restricted by 40% and their diets contained 13.1% corn oil. Incidence of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors was 80% in rats fed ad libitum and 20% in those fed the calorie-restricted diets. Incidence of 1,2-dimethylhydrazine (DMH)-induced colon tumors was 100% in rats fed ad libitum and 53% in those whose caloric intake was restricted by 40%. The tumor yield (tumors per tumor-bearing rat) was significantly lower in rats on caloric restriction. In another series, rats were fed diets containing 5, 15 or 20% corn oil ad libitum or were fed calorie-restricted (by 25%) diets which provided 20 or 26.6% corn oil (therefore, the same absolute amount of fat was consumed in each of the pair-fed groups). Tumor incidence and tumor yield in the two calorie-restricted groups were similar to those seen in the rats fed 5% fat ad libitum; tumor burden (total g of tumor) was 45-65% lower in the calorie-restricted rats. The data suggest that caloric intake is a more stringent determinant of tumor growth than fat intake. MH - Animal ; Caloric Intake ; Colonic Neoplasms/*ETIOLOGY/PATHOLOGY ; Comparative Study ; *Diet ; Diet, Reducing ; Dietary Fats/ *ADVERSE EFFECTS ; Female ; Male ; Mammary Neoplasms, Experimental/*PATHOLOGY ; Rats ; Rats, Inbred F344 ; Rats, Inbred Strains ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. ; 9,10-Dimethyl-1,2-Benzanthracene SO - Lipids 1986 Apr;21(4):272-4 21 UI - 86213772 AU - Cohen LA ; Choi K ; Weisburger JH ; Rose DP TI - Effect of varying proportions of dietary fat on the development of N-nitrosomethylurea-induced rat mammary tumors. AB - The influence of diets varying in their relative proportions of dietary fat on N-nitrosomethylurea (NMU)-induced mammary tumorigenesis, was assessed. Animals were initiated on day 50 of age with 25 mg/kg NMU and then placed on casein-based AIN-76A diets containing 5, 10, 16 and 23% corn oil (wt/wt). There were 30 animals/group and the experiment was terminated 22 weeks post-NMU. It was found that animals fed diets containing 16 and 23% corn oil exhibited tumor incidences between 2 and 3 times that of animals fed diets containing 5 and 10% corn oil. No differences in tumor incidence could be detected between the 5 and 10% groups or the 16 and 23% groups, suggesting that a threshold occurs at some point between 10 and 16% fat (or 20 and 33% of total calories as fat). The results of this study suggest that the tumor-promoting effects of dietary fat are manifested in terms of a threshold, rather than a linear dose-response effect. MH - Animal ; Breast Neoplasms/PREVENTION & CONTROL ; Cocarcinogenesis ; Dietary Fats/*ADMINISTRATION & DOSAGE ; Female ; Human ; Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED ; Methylnitrosourea ; Mice ; Rats ; Rats, Inbred F344 ; Risk ; Support, U.S. Gov't, P.H.S. SO - Anticancer Res 1986 Mar-Apr;6(2):215-8 22 UI - 86189494 AU - Ip C ; White G TI - BCG-modulated mammary carcinogenesis is dependent on the schedule of immunization but is not affected by dietary fat. AB - The present study was designed to study the effect of dietary fat intake on the modulation of dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in rats injected with the methanol extract residue of Bacillus Calmette-Guerin (MER-BCG). Rats were maintained on either a 5% or a 20% corn oil diet for the entire duration of the experiment. When MER-BCG was administered 2 and 3 weeks before DMBA, mammary tumorigenesis was suppressed in the 2 dietary groups with different levels of fat intake. This was in contrast to when MER-BCG was administered 3 and 5 weeks after DMBA; in this case the development of mammary tumors was noticeably enhanced regardless of the fat intake of the host. The magnitude of inhibition or increase by MER-BCG was similar in animals fed either fat level, although a high fat diet consistently stimulated mammary tumorigenesis in the 2 experiments. In vitro assays on T cell mitogen-induced blastogenesis and natural killer cell activity in splenocytes isolated from the untreated rats showed that dietary fat failed to elicit any differential response in these immune functions. MH - Animal ; BCG Vaccine/*ADMINISTRATION & DOSAGE ; *Dietary Fats ; Female ; Killer Cells, Natural/IMMUNOLOGY ; Lymphocyte Transformation ; Mammary Neoplasms, Experimental/CHEMICALLY INDUCED/IMMUNOLOGY/*PREVENTION & CONTROL ; Rats ; Rats, Inbred Strains ; Spleen/IMMUNOLOGY ; Support, U.S. Gov't, P.H.S. ; 9,10-Dimethyl-1,2-Benzanthracene SO - Cancer Lett 1986 Apr;31(1):87-96 23 UI - 86183757 AU - Newman SC ; Miller AB ; Howe GR TI - A study of the effect of weight and dietary fat on breast cancer survival time. AB - Female breast cancer patients who had participated in a case-control study conducted during 1973-1975 were followed up, using record linkage to the Statistics Canada mortality data base, to the end of 1980. A number of variables recorded for the case-control study, in particular body weight and daily intake of dietary fat near the time of diagnosis, were examined to see if they had any bearing on breast cancer mortality. The data were analyzed using the methods of Mantel and Cox. Dietary fat was not found to be related to patient survival. However, cases with greater than average body weight experienced a shortened survival time. MH - Adult ; Aged ; Body Weight ; Breast Neoplasms/*MORTALITY ; Death Certificates ; Diet Surveys ; Dietary Fats/*ADVERSE EFFECTS ; Epidemiologic Methods ; Female ; Human ; Medical Record Linkage ; Middle Age ; Prognosis ; Statistics ; Support, Non-U.S. Gov't ; Time Factors SO - Am J Epidemiol 1986 May;123(5):767-74 24 UI - 86166145 AU - Bieber MA TI - Lack of oestrogen-like activity in commercially refined vegetable oils. AB - Commercially refined corn, safflower, sunflower and soya-bean oils, as well as well as lard and beef tallow, were fed to pre-pubertal female mice at a level of 5 or 20% of a semi-synthetic diet to assess whether they exhibited any oestrogen-like activity, as measured by changes in uterine weight or in the ratio of uterine weight to body weight. No measurable oestrogen-like activity was observed, in contrast to the effects in positive-control animals treated with 5, 10 or 15 ppb diethylstilboestrol. This finding contradicts an earlier report in the literature. It also shows that oestrogen-like activity in a commercially refined oil is not likely to be a variable in the complex mechanism of the dietary modulation of induced breast-tumour growth. MH - Animal ; Breast Neoplasms/ETIOLOGY ; Dietary Fats/ADVERSE EFFECTS ; Estrogens/*PHARMACODYNAMICS ; Female ; Mice ; Mice, Inbred ICR ; Oils/*PHARMACODYNAMICS ; Organ Weight/DRUG EFFECTS ; Uterus/ DRUG EFFECTS SO - Food Chem Toxicol 1986 Mar;24(3):251-3 25 UI - 86165888 AU - Bauer RL TI - Office techniques to maintain the health of aging patients. AB - The fecal occult blood test is safe and inexpensive; however, diet, medications, desiccation of the sample, and delay in developing the specimen may affect results. If the test is used, six separate samples, two from each of three consecutive bowel movements, should be examined to obtain optimum results. Serum cholesterol need not be assessed routinely in geriatric patients. Dietary restriction of fats is a necessity only in the context of a weight reduction diet. MH - Accident Prevention ; Aged ; Antihypertensive Agents/THERAPEUTIC USE ; Breast Neoplasms/PREVENTION & CONTROL ; Cerebrovascular Disorders/PREVENTION & CONTROL ; Cervix Neoplasms/PREVENTION & CONTROL ; Cholesterol, Dietary/METABOLISM ; Clinical Trials ; Colonic Neoplasms/PREVENTION & CONTROL ; Coronary Disease/ PREVENTION & CONTROL ; Female ; *Geriatrics ; Human ; Hypertension/DRUG THERAPY/PREVENTION & CONTROL ; Influenza Vaccine/THERAPEUTIC USE ; Lung Neoplasms/PREVENTION & CONTROL ; Male ; Middle Age ; Occult Blood ; Pneumonia/PREVENTION & CONTROL ; Pneumonia, Lobar/PREVENTION & CONTROL ; *Preventive Medicine ; Prostatic Neoplasms/PREVENTION & CONTROL ; Sigmoidoscopy ; Smoking/PREVENTION & CONTROL SO - Geriatrics 1986 May;41(5):91-2, 96-102, 106-7 26 UI - 86133205 AU - Leung KH ; Ip MM TI - Effect of dietary polyunsaturated fat and 7,12-dimethylbenz(a)-anthracene on rat splenic natural killer cells and prostaglandin E synthesis. AB - Dietary polyunsaturated fat has been shown to stimulate mammary tumorigenesis induced in rats by 7,12-dimethylbenz(a)anthracene (DMBA). Studies were undertaken to investigate the effect of polyunsaturated fat and DMBA on splenic natural killer (NK) activity and prostaglandin E (PGE) synthesis. In a first experiment, splenic NK activity at 33, 55, 75, and 110 days of age was measured in Sprague-Dawley rats fed 0.5% low fat (LF), 5% normal fat (NF), or 20% high fat (HF) corn oil diets from 23 days of age. At 55 days of age, half of the rats from the 75 and 110 day age groups were given 5 mg DMBA. Ten days after the initiation of the diets splenic NK activity against YAC-1 lymphoma was decreased from 50% cytotoxicity in rats fed NF diet to 21% cytotoxicity in rats fed HF diet, but was not affected by LF feeding. No difference in NK activity was observed among the groups at the later time periods. DMBA had no effect on NK activity at 20 or 55 days after its administration. In a second experiment, where DMBA (15 mg/rat) was given to half of the rats at 50 days of age and NF or HF diets were started 3 days later, NK activity was 35% in rats fed NF diet and 21% in rats fed HF diet, 5 days after the diets were started. No difference in NK activity in rats fed either diet was observed at later time periods. DMBA decreased both NK activity and spleen cellularity transiently. In both experiments, PGE synthesis by spleen cells cultured for 18 h was not affected by dietary fat intake, but was slightly increased 3 days after DMBA administration. Results from these experiments suggest that the stimulation of DMBA-induced mammary tumorigenesis by polyunsaturated fat and by DMBA itself may possibly be mediated by a transient decrease in splenic NK cell activity. MH - Animal ; Dietary Fats/*ADVERSE EFFECTS ; Fatty Acids, Unsaturated/ *ADVERSE EFFECTS ; Female ; Killer Cells, Natural/DRUG EFFECTS/ *IMMUNOLOGY ; Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED/ IMMUNOLOGY ; Prostaglandins E/*BIOSYNTHESIS ; Rats ; Spleen/ CYTOLOGY/IMMUNOLOGY ; Support, U.S. Gov't, P.H.S. ; 9,10-Dimethyl-1,2-Benzanthracene/*PHARMACODYNAMICS SO - Cancer Immunol Immunother 1986;21(2):161-3 27 UI - 86127279 AU - Wysowski DK ; Goldberg EL ; Comstock GW ; Diamond EL TI - A study of a possible association between breast cancer and gallbladder disease. AB - Because gallstones and breast cancer were reported to have several of the same risk factors, a study was conducted in Washington County, Maryland to determine if women with breast cancer have an increased risk of prior gallbladder disease. Living white female breast cancer cases (n = 133), who were diagnosed from 1973 to 1983, were identified from the county's cancer registry and interviewed along with an equal number of sex-, race-, and age-matched controls about a history of gallbladder disease and other risk factors. Medical records were used to verify a history of gallbladder disease in interviewed cases and controls and to search for a diagnosis of gallbladder disease in 52 white female breast cancer cases who were diagnosed and died between 1974 and 1983, and 52 matched controls. No difference was found in gallbladder disease frequency among living or deceased cases and their matched controls. The results confirm the known association of several risk factors with breast cancer and with gallbladder disease, but most of the risk factors hypothesized to be the same for the two diseases were not the same. However, an unexpectedly strong association was found between gallbladder disease and history of myocardial infarction; this result deserves further study. MH - Aged ; Breast Neoplasms/*COMPLICATIONS/MORTALITY ; Cholecystitis/ COMPLICATIONS/OCCURRENCE ; Cholelithiasis/COMPLICATIONS/ OCCURRENCE ; Dietary Fats/ADMINISTRATION & DOSAGE ; Female ; Gallbladder Diseases/*COMPLICATIONS/OCCURRENCE ; Human ; Interviews ; Maryland ; Middle Age ; Myocardial Infarction/ COMPLICATIONS ; Obesity/COMPLICATIONS ; Registries ; Risk SO - Am J Epidemiol 1986 Mar;123(3):532-43 28 UI - 86116250 AU - Aylsworth CF ; Cullum ME ; Zile MH ; Welsch CW TI - Influence of dietary retinyl acetate on normal rat mammary gland development and on the enhancement of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumorigenesis by high levels of dietary fat. AB - The effect of high levels of dietary fat and retinyl acetate (ROA) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumor development and growth was examined. Female Sprague-Dawley rats, 51-53 days of age, were treated ig with 5 mg DMBA. At 55-57 days of age, the animals were divided into the following dietary treatment groups: A) 4.5% fat [control fat (CF)]; B) CF + 1.0 mmol ROA/kg diet (CF + ROA); C) 20.0% fat [high fat (HF)]; and D) HF + ROA. HF diets significantly increased mammary tumor multiplicity, with or without ROA, but did not significantly influence mammary tumor growth. ROA treatment reduced mammary tumor multiplicity regardless of the level of dietary fat and inhibited mammary tumor growth in the presence of normal levels of dietary fat. High levels of dietary fat did not significantly influence normal mammary gland growth and development. ROA significantly decreased normal mammary gland growth and development regardless of the level of dietary fat. Blood retinoids in rats fed ROA were primarily in the form of retinyl esters, i.e., retinyl linoleate, retinyl palmitate-oleate, and retinyl stearate. Free retinol levels in blood were not significantly influenced by ROA feeding. Blood retinyl ester levels were lower in rats fed the HF + ROA diet as compared to rats fed the CF + ROA diet. MH - Animal ; Body Weight/DRUG EFFECTS ; Cocarcinogenesis ; Dietary Fats/*ADMINISTRATION & DOSAGE/PHARMACODYNAMICS ; Female ; Mammae/ *DRUG EFFECTS/GROWTH & DEVELOPMENT ; Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED/PATHOLOGY ; Rats ; Rats, Inbred Strains ; Retinoids/BLOOD ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S. Gov't, P.H.S. ; Time Factors ; Vitamin A/*ANALOGS & DERIVATIVES/BLOOD/PHARMACODYNAMICS ; *9,10-Dimethyl-1,2-Benzanthracene SO - JNCI 1986 Feb;76(2):339-45 29 UI - 86116249 AU - Boissonneault GA ; Elson CE ; Pariza MW TI - Net energy effects of dietary fat on chemically induced mammary carcinogenesis in F344 rats. AB - The effect of net energy, as distinct from kilocalorie intake or the percent of fat in the diet, on 7,12-dimethylbenz[a]anthracene [(DMBA) CAS: 57-97-6]-induced mammary tumorigenesis in female inbred F344 rats was investigated. Rats were fed a 5% corn oil diet from weaning until DMBA administration, when they were switched to one of three dietary regimens: 5% corn oil diet, low-fat diet fed ad libitum (LF); 30% corn oil diet, high-fat diet fed ad libitum (HF); or 30% corn oil diet fed at a level providing a calculated net energy equivalent to the group on LF [high-fat diet fed at a restricted level (HF-R)]. Calculated relative net energy values of the amounts of diet actually consumed by the groups on HF-R, LF, and HF were, respectively, 0.90, 1.00, and 1.07 (kcal equivalent to 34.1, 42.2, and 40.8, respectively). Weight gain for the groups on LF and HF-R was the same throughout the experiment (24 wk), while rats on HF weighed significantly more at 6 weeks and thereafter. Body composition analyses at 24 weeks established that the groups on HF and HF-R were equivalent in fat: protein ratio, whereas the group on LF had about 35% less body fat and 15% more body protein. Carcass energy was in the following order for rats in these diet groups: HF greater than HF-R greater than LF. At 24 weeks, tumor incidences for the groups on HF, LF, and HF-R were, respectively, 73, 43, and 7%. These data indicated that tumor appearance does not depend on the percent fat in the diet per se but rather on a complex interaction involving energy intake, energy retention, and body size. MH - Animal ; Body Composition ; Body Weight ; Caloric Intake ; Cocarcinogenesis ; Dietary Fats/*METABOLISM/PHARMACODYNAMICS ; Energy Metabolism ; Female ; Mammary Neoplasms, Experimental/ *CHEMICALLY INDUCED/METABOLISM ; Rats ; Rats, Inbred F344 ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S. Gov't, P.H.S. ; Time Factors ; 9,10-Dimethyl-1,2-Benzanthracene SO - JNCI 1986 Feb;76(2):335-8 30 UI - 86079172 AU - Sylvester PW ; Ip C ; Ip MM TI - Effects of high dietary fat on the growth and development of ovarian-independent carcinogen-induced mammary tumors in rats. AB - This study examined the influence of high dietary fat intake on the development of ovarian-independent mammary tumors in both vehicle-treated controls and rats made deficient in estrogen and prolactin during tumor induction. The majority of 7,12-dimethylbenz(a) anthracene (DMBA)-induced mammary tumors in rats are dependent on estrogen and prolactin for growth, and suppression of prolactin and estrogen at the time of tumor initiation causes a reduction in tumor incidence and increase in tumor latency. However, the majority of mammary tumors which do develop in these animals exhibit ovarian-independent growth. Sprague-Dawley rats were given 7.5 mg DMBA p.o. at 57 days of age. Starting 1 day prior to and continuing for 7 days after DMBA administration, rats were given daily injection of vehicle or the combination of tamoxifen (20 micrograms/rat) plus bromocryptine (5 mg/kg). At the end of drug treatment, rats in each treatment group were equally divided and placed on normal fat (5% corn oil) or high fat (20% corn oil) diets for the duration of the experiment. Vehicle-treated rats were ovariectomized 27 wk and drug-treated rats 47 wk after DMBA administration to determine tumor ovarian dependency. Vehicle-treated rats fed high fat diets showed significant increases in mammary tumor incidence and number as compared to similarly treated rats fed a normal fat diet, with approximately 80% of the tumors in each group being ovarian dependent. Likewise, tamoxifen-bromocryptine-treated rats fed a high fat diet showed a significant enhancement in mammary tumor number, although not incidence, as compared to similarly treated rats fed a normal diet. Tumors in these drug-treated groups displayed essentially the same incidence of ovarian dependence (23%). Tamoxifen-bromocryptine-treated groups displayed a 2-fold increase in latency of tumor appearance as compared to vehicle-treated controls; however, this long latency was not reduced when these rats were fed a high fat diet. These results demonstrate that high dietary fat stimulates ovarian-dependent and -independent mammary tumorigenesis in rats but does not influence the hormonal responsiveness of these tumors. MH - Animal ; Bromocriptine/PHARMACODYNAMICS ; Dietary Fats/*ADVERSE EFFECTS ; Estrogens/PHYSIOLOGY ; Female ; Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED ; Ovariectomy ; Ovary/PHYSIOLOGY ; Prolactin/PHYSIOLOGY ; Rats ; Support, U.S. Gov't, P.H.S. ; Tamoxifen/PHARMACODYNAMICS ; 9,10-Dimethyl-1,2-Benzanthracene SO - Cancer Res 1986 Feb;46(2):763-9 31 UI - 86079171 AU - Sylvester PW ; Russell M ; Ip MM ; Ip C TI - Comparative effects of different animal and vegetable fats fed before and during carcinogen administration on mammary tumorigenesis, sexual maturation, and endocrine function in rats. AB - The purpose of this investigation was to determine whether diets high in animal or vegetable fat affected mammary tumorigenesis when fed to rats only prior to and during the initiation phase of carcinogenesis. Weanling 21-day-old female Sprague-Dawley rats were divided into different dietary treatment groups and were allowed to feed and libitum on one of the following diets: 5% (normal fat) corn oil; 20% (high fat) corn oil; 20% palm oil; 20% beef tallow; or 20% lard. At 52 days of age, all rats were given p.o. 7.5 mg 7,12-dimethylbenz(a)anthracene (DMBA). One week following DMBA administration, all rats were switched to the 5% corn oil control diet and were maintained on this diet for the duration of the experiment. Rats fed a 20% lard diet during the treatment period showed a significant increase in mammary tumor incidence and number 19 weeks after DMBA administration, when compared to all other dietary treatment groups. Rats fed a 20% beef tallow diet during this same time period also demonstrated enhanced mammary tumor development, during the 10- to 19-week time period after DMBA. Mammary tumor development in rats fed 20% corn oil or palm oil diets during this treatment period was similar to that of normal fat controls. Estrogens are potent stimulators of mammary tumor growth and development in rats. Because mammary tumorigenesis was enhanced in rats fed high animal, but not vegetable fat diets, it was possible that estrogens present in animal fat might be responsible for this stimulation. Further studies demonstrated however, that increased mammary tumorigenesis in rats fed diets high in animal fat could not be explained on the basis of endocrine stimulation. Average day of vaginal opening for all groups fed 20% fat diets was similar and occurred earlier than in normal fat controls. In addition, 50- to 65-day-old rats in the different dietary treatment groups showed no differences in basal or surge levels of serum prolactin, luteinizing hormone, or estradiol. Rat diestrus uterine weight also showed no significant differences among dietary treatment groups. Thus diets containing high levels of animal fat caused little if any increased estrogenic activity in rats. In conclusion, high dietary intake of lard and beef tallow, but not vegetable fat, fed from weaning until only 1 week after DMBA administration, significantly enhances mammary tumorigenesis in rats. The mechanism(s) by which animal fat induces this stimulation is not clear, but it does not appear to result from endogenous or exogenous endocrine stimulation. MH - Animal ; Dietary Fats/*ADVERSE EFFECTS ; Estrus ; Female ; Mammary Neoplasms, Experimental/CHEMICALLY INDUCED ; Neoplasms, Experimental/*CHEMICALLY INDUCED ; Prolactin/*BLOOD ; Rats ; *Sex Maturation ; Support, U.S. Gov't, P.H.S. ; Time Factors SO - Cancer Res 1986 Feb;46(2):757-62