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PubMed1984

Diet and the epidemiology of human breast cancer.

There are substantial data on breast tumorigenesis in animals that suggest that diet may be an important factor in human breast cancer etiology. The promotional effects of dietary fat, and, in particular, unsaturated fats, on mammary tumors in rodents is well established. The geographic distribution of breast cancer in humans correlates with international differences in average fat intake. Differences in dietary habits among populations in the United States and their breast cancer risk also have been observed. In the United States, the trend has been toward increased total fat consumption and increased use of polyunsaturated fats. However, breast cancer incidence among white women in the United States has changed very little. Case-control studies of dietary intake and breast cancer risk have shown inconsistent results, and prospective studies of breast cancer mortality and serum cholesterol and serum lipids show no differences in risk between women with high levels of cholesterol and serum lipids compared with women with low levels. Laboratory studies also suggest the possibility that natural inhibitors of breast cancer may occur in the diet as well. Antioxidants, inducers of microsomal enzyme activity, and retinoids, all have been implicated in the metabolic epidemiology of breast cancer. Research results at Roswell Park memorial Institute have associated lower levels of intake of dietary vitamin A with a slightly elevated risk of breast cancer. To date, the epidemiologic data do not indicate with confidence that any specific dietary risk factor may be associated with breast cancer risk in the United States population. Additional epidemiologic studies on inhibition or promotion of breast cancer following the leads of previous laboratory research may clarify the nature and practical significance of the relationship between diet and breast cancer.

Adolescent↗
PubMed1977

Effects of diet composition on serum levels of insulin, thyroxine, triiodothyronine, growth hormone, and corticosterone in rats.

These studies were designed to determine the effects of diet composition on serum insulin, triiodothyronine, thyroxine, growth hormone, and corticosterone and to correlate these hormones with feed intake, body weight, and adipose tissue weight in rats. Experimental diets were fed for a period of 4 weeks. The experimental dietary groups were as follows: high starch (HST), high glucose (HG), high sucrose (HSU), high protein (HP), high saturated fat (HFS), and higher unsaturated fat (HFU). Serum glucose concentrations were not significantly different among any of the groups. The HST, HSU and HG diets produced the highest serum insulin. Serum thyroid hormone levels were highest in rats fed high fat diets. No significant differences in serum growth hormone or corticosterone levels were noted among the dietary groups. There was a tendency for rats fed a high protein diet to have higher concentration of corticosterone. However, there were no significant differences detected. There was a significant negative correlation between serum corticosterone and ovarian adipose tissue weight. It is concluded from these studies that these types of dietary manipulation have a significant effect on endocrine status and body fat deposition.

Adipose Tissue↗
PubMed2006

Dietetic guidelines on food and nutrition in the secondary prevention of cardiovascular disease - evidence from systematic reviews of randomized controlled trials (second update, January 2006).

AIM: To update dietetic guidelines based on systematic review evidence on dietary advice to prevent further events in people with existing cardiovascular disease (CVD) (secondary prevention). METHODS: The Cochrane Library, MEDLINE and EMBASE were comprehensively searched to January 2005 for systematic reviews on aspects of diet and heart health. Reviews were included if they searched systematically for randomized controlled trials relating to diet and secondary prevention of CVD. Each review was critically appraised by at least two members of the UK Heart Health and Thoracic Dietitians Group. The quality and results of each review were discussed and summarized at a group meeting. RESULTS: Evidence-based strategies that reduce cardiovascular events in those with CVD include reduction in saturated fat and substitution with unsaturated fats. Individuals who have suffered a myocardial infarction may also benefit from adopting a Mediterranean type diet and increasing intake of omega 3 fats, but it is not clear whether they are beneficial for all patients with CVD. There is no systematic review evidence to support the use of antioxidant vitamins supplements, low glycaemic index diets, or homocysteine lowering therapies in this group. CONCLUSION: There remains good evidence that reducing saturated fat reduces morbidity in patients with CVD. This advice is consistent for most manifestations of CVD, with the addition of Mediterranean dietary advice and increased omega 3 fats for those who have had a myocardial infarction.

Antioxidants↗
PubMed2001

Manganese absorption and retention in rats is affected by the type of dietary fat.

There is evidence that manganese (Mn) metabolism may be altered by the form and amount of dietary fat. Also, iron (Fe) absorption is greater with saturated fats, as compared to polyunsaturated fatty acids (PUFAs). The absorption of Fe and Mn are interrelated in many aspects; therefore, the form of dietary fat may indirectly alter Mn absorption. The reported studies were conducted to determine whether saturated fat, as compared to unsaturated fat, affected Mn absorption, retention, and metabolism. In experiment I, adult rats were fed diets containing either 0.7 or 100.4 microg/g Mn with the fat source as high-linoleic safflower oil or stearic acid. After 2 wk of equilibration, the animals were fed a test meal of 54Mn followed by whole-body counting for 10 d. Manganese absorption was significantly (p < 0.05) lower in the stearic acid group (0.9-4.8%) than in the safflower oil group (20-33.8%); however, the biological half-life was shorter in the safflower oil group. Retention of 54Mn and total Mn was always significantly (p < 0.05) greater in the safflower oil group when dietary Mn was low, but it was the same when dietary Mn was high. In experiment II, weanling rats were fed 1.3, 39.3, or 174.6 microg Mn/g and either stearate, high-oleic safflower oil or high-linoleic safflower oil for 8 wk. Long-term feeding of the stearate and low Mn-containing diet resulted in a significant (p < 0.0001) reduction in heart superoxide dismutase activity and kidney and liver Mn concentrations compared to the other diets. These data show that stearic acid inhibitits Mn absorption, but it may not inhibit Mn retention when dietary Mn is high.

Animals↗
PubMedDate not supplied

Effect of dietary fat and cholesterol on dimethylbenz[a]-anthracene-induced mammary tumorigenesis in Sprague-Dawley rats.

The effect of dietary fats and cholesterol on dimethylbenz[a]-anthracene-induced mammary tumorigenesis was studied in female Sprague-Dawley rats. When the dietary fat source (at the 5% level) was palm oil (saturated fat) or corn oil (unsaturated fat), dietary cholesterol at the 0.2% level increased the tumor number of rats fed corn oil, but not those fed palm oil. Perilla oil (rich in alpha-linolenic acid) reduced tumor development as compared with safflower oil (rich in linoleic acid), but again dietary cholesterol at the 0.5% level diminished the favorable effect of n-3 polyunsaturated fatty acid (PUFA). The adverse effect of cholesterol was also observed in the n-6 PUFA fat. The promotive effect of dietary cholesterol was not necessarily associated with the change in the production of prostaglandin E2 by the tumor tissue or in the immunopotentiation. These results at least stress that the contrasting effects of dietary fats should be carefully evaluated whether cholesterol is present simultaneously or not.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

Effects of dietary menhaden oil on mucosal adaptation after small bowel resection in rats.

BACKGROUND/AIMS: Adaptive hyperplasia of the small intestine is important in the outcome of short bowel syndrome. Previous studies have shown that long-chain fats stimulate this process. In the present study, the trophic effects of dietary menhaden oil, a highly unsaturated fat source, on mucosal adaptation following small bowel resection in rats was evaluated. METHODS: Thirty weanling Sprague-Dawley rats and their controls were fed diets containing fats provided primarily as menhaden oil, safflower oil, or beef tallow. After 4 weeks, animals underwent a 70% jejunoileal resection. Mucosal mass, DNA, protein, and sucrase levels were assessed 14 days after a 70% jejunoileal resection or control feeding. Serum fatty acid composition and several gastrointestinal hormone levels were measured. RESULTS: Resected animals fed menhaden oil showed a marked increase in mucosal weight, DNA, and protein levels compared with rats fed the other fat sources. Enteroglucagon level was increased in all resected groups, but least increased in the menhaden-fed animals. In contrast, peptide YY concentrations were most increased in animals fed menhaden oil. CONCLUSIONS: Menhaden oil appears more effective in inducing intestinal adaptation than less highly unsaturated fats. Analysis of gastrointestinal hormones revealed no clear-cut explanation for this finding, other than a modest but associated increase in peptide YY levels.

Adaptation, Physiological↗
PubMed1981

The influence of dietary fat and non-specific immunotherapy on carcinogen-induced rat mammary adenocarcinoma.

The incidence of mammary adenocarcinoma in Sprague-Dawley female rats, caused by the carcinogen 7,12-dimethylbenz(alpha)anthracene, was influenced by the level of dietary fat fed after exposure to carcinogen. Carcinogen was given by stomach tube to 50-day-old rats, and tumors were evaluated when rats were 9 months old. Rats on diets containing 20% unsaturated fat had a tumor incidence of 97%, while rats changed to a low-fat diet (2% unsaturated fat) three or four weeks after exposure to the carcinogen had an incidence of 45%. Some rats on each diet were given two treatments with the methanol extraction residue of Bacillus Calmette-Guerin, either three and five weeks after carcinogen or four and six weeks after carcinogen. Tumor incidence in the treated group and the untreated group was the same when rats were maintained on the high-fat diet, but tumors in the treated group were larger and the disease was more severe by histological criteria. These tumors were more anaplastic and many were extensively infiltrated with lymphocytes compared to the untreated group. Tumor incidence was significantly lower in rats changed to the low-fat diet (45%) than in those on the high-fat diet (97%), and tumor incidence was reduced to 20% when rats changed to the low-fat diet were treated with methanol extraction residue. The treated group had less severe disease than the untreated group on the low-fat diet. Only half the tumor-bearing rats in this group had malignant tumors, and none were invasive. Methanol extraction residue protected most rats on the low-fat diet against mammary adenocarcinoma, and reduced the severity of disease in those rats that did develop tumors. Methanol extraction residue treatment provided no protection, and even increased the severity of disease, in rats on the high-fat diet.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Association of dietary intake of fat and fatty acids with risk of breast cancer.

CONTEXT: High intakes of fat and specific fatty acids, including total, animal, saturated, polyunsaturated, and trans-unsaturated fats, have been postulated to increase breast cancer risk. OBJECTIVE: To determine whether intakes of fat and fatty acids are associated with breast cancer. DESIGN AND SETTING: Cohort study (Nurses' Health Study) conducted in the United States beginning in 1976. PARTICIPANTS: A total of 88795 women free of cancer in 1980 and followed up for 14 years. MAIN OUTCOME MEASURE: Relative risk (RR) of invasive breast cancer for an incremental increase of fat intake, ascertained by food frequency questionnaire in 1980, 1984, 1986, and 1990. RESULTS: A total of 2956 women were diagnosed as having breast cancer. Compared with women obtaining 30.1% to 35% of energy from fat, women consuming 20% or less had a multivariate RR of breast cancer of 1.15 (95% confidence interval [CI], 0.73-1.80). In multivariate models, the RR (95% CI) for a 5%-of-energy increase was 0.97 (0.94-1.00) for total fat, 0.98 (0.96-1.01) for animal fat, 0.97 (0.93-1.02) for vegetable fat, 0.94 (0.88-1.01) for saturated fat, 0.91 (0.79-1.04) for polyunsaturated fat, and 0.94 (0.88-1.00) for monounsaturated fat. For a 1% increase in energy from trans-unsaturated fat, the values were 0.92 (0.86-0.98), and for a 0.1% increase in energy from omega-3 fat from fish, the values were 1.09 (1.03-1.16). In a model including fat, protein, and energy, the RR for a 5% increase in total fat, which can be interpreted as the risk of substituting this amount of fat for an equal amount of energy from carbohydrate, was 0.96 (95% CI, 0.93-0.99). In similar models, no significant association of risk was evident with any major types of fat. CONCLUSION: We found no evidence that lower intake of total fat or specific major types of fat was associated with a decreased risk of breast cancer.

Adult↗
PubMed2003

Increased translocation of cardiac protein kinase C beta2 accompanies mild cardiac hypertrophy in rats fed saturated fat.

Signal transduction through protein kinase C (PKC) beta2 may modulate cardiac hypertrophy in pressure-overloaded rat myocardium. Because PKC beta2 can be activated by fatty acids and diacylglycerol, we hypothesized that altering the level and type of dietary fat might modulate cardiac PKC activation and stimulate hypertrophy in otherwise normal rat myocardium. Male Sprague-Dawley rats (n = 32) were randomly assigned to either a low fat [10% total energy intake (TEI)] or high fat diet (40% TEI) based on corn or coconut oil as a source of saturated or unsaturated fat. After 40 d of isoenergetic diet consumption, the heart/body weight ratio was slightly greater in rats fed saturated fat diets compared with those fed unsaturated fat (P = 0.05). Increased activation of PKC beta2, as evidenced by greater membrane translocation, was also observed in all rats fed saturated fat diets (P < 0.01). PKC alpha, beta1 and epsilon did not change. These results suggest that dietary fat type can alter PKC beta2 activation in the heart, and exert a mild hypertrophic effect on the heart.

Animals↗
PubMed1992

Dietary fat and the development of pancreatic cancer.

Pancreatic cancer is the fifth most common cause of death due to cancer. Except for an association with cigarette smoking, its etiology is poorly understood. Because of the dearth of epidemiological clues as to causation, studies with experimental animal models assume greater importance. Rodent models of pancreatic cancer indicate that while dietary fat per se does not cause pancreatic cancer, it does enhance or promote tumor development. Subsequent to treatment with a pancreatic carcinogen, high intakes of dietary unsaturated fats of the n-6 series, but not saturated fats, enhance or promote tumor development. A requisite level of linoleic acid is needed for this promotion. Fats of the n-3 series (e.g., certain fish oils) are inhibitory to tumor growth. Promotion by dietary fats appears only partly related to the high caloric content of fat. Mechanistically, certain dietary unsaturated fats appear to selectively enhance the growth rate of carcinogen-induced, pre-cancerous lesions. Irrespective of precise understanding of mechanisms of promotion, it appears possible to intervene in the process of cancer development and reduce the burden of cancer. Experimentally, this may be accomplished by decreasing total fat intake, decreasing caloric intake, increasing exercise or increasing the intake of n-3 fatty acids.

Animals↗
PubMed1991

Effects of fat and fiber on human colon cancer xenografted to athymic nude mice.

The effects of unsaturated fat and fiber (cellulose) on the growth of human colon cancer explanted to athymic nude mice was evaluated. Eighty-seven male nude mice bearing xenografts of human HT29 or WiDr colon cancer were divided into three groups of equal weight and tumor volume. Each group was fed one of three diets: normal fat/no fiber (N/N), high fat/no fiber (H/N) or high fat/high fiber (H/H). To equalize caloric intake, animals in the H/N group received 4 g of food per day and the other animals were fed 5 g of food per day. At sacrifice tumor volume and weight was recorded, and tumors were analyzed for protein and DNA content and ornithine decarboxylase activity. Tumor volume, weight, and protein were greater in the H/N group compared to the N/N group for both colon cancer cell lines. Tumor DNA content was greater in the HT29 H/N group compared to the N/N group (P less than 0.05) and tumor ornithine decarboxylase activity in the WiDr H/N group was greater than the N/N animals (P less than 0.002). The tumor growth-promoting effects of the high unsaturated fat diet were attenuated by the addition of fiber. Animal weight was higher in the H/N group compared to the N/N and H/H groups. This study suggested that a high-fat diet stimulated and fiber decreased the growth of human colon cancer explanted to athymic nude mice. The growth-promoting effects of a high-fat diet in colorectal cancer may be due in part to a circulating trophic factor since these tumors were remote from the large intestine.

Animals↗
PubMed2003

Role of nuclear receptors in the regulation of gene expression by dietary fatty acids (review).

Long chain fatty acids, derived either from endogenous metabolism or by nutritional sources play significant roles in important biological processes of membrane structure, production of biologically active compounds, and participation in cellular signaling processes. Recently, the structure of dietary fatty acids has become an important issue in human health because ingestion of saturated fats (containing triglycerides composed of saturated fatty acids) is considered harmful, while unsaturated fats are viewed as beneficial. It is important to note that the molecular reason for this dichotomy still remains elusive. Since fatty acids are important players in development of pathology of cardiovascular and endocrine system, understanding the key molecular targets of fatty acids, in particular those that discriminate between saturated and unsaturated fats, is much needed. Recently, insights have been gained on several fatty acid-activated nuclear receptors involved in gene expression. In other words, we can now envision long chain fatty acids as regulators of signal transduction processes and gene regulation, which in turn will dictate their roles in health and disease. In this review, we will discuss fatty acid-mediated regulation of nuclear receptors. We will focus on peroxisome proliferators-activated receptors (PPARs), liver X receptors (LXR), retinoid X receptors (RXRs), and Hepatocyte Nuclear Factor alpha (HNF-4alpha), all of which play pivotal roles in dietary fatty acid-mediated effects. Also, the regulation of gene expression by Conjugated Linoleic Acids (CLA), a family of dienoic fatty acids with a variety of beneficial effects, will be discussed.

Amino Acid Sequence↗
PubMed1992

Dietary fat, calories, and mammary gland tumorigenesis.

In this communication, a vast array of studies designed to examine the relationship between dietary fat and experimental mammary gland tumorigenesis was reviewed and critiqued. It is clear, as reported by many laboratories, that as the fat content of the diet is increased from a low or standard level to a high level, a consistent and substantial increase in the development of rodent mammary gland tumors is observed. The longer the duration the high-fat diet is fed, the greater the enhancing effect on tumorigenesis. Furthermore, the stimulatory effect of a high-fat diet is observed even when fed commencing late in an animal's life. A multitude of studies also have provided evidence that the type of fat can markedly influence the development of rodent mammary gland tumors. In general, high dietary levels of unsaturated fats (e.g., corn oil, sunflower-seed oil) stimulate this tumorigenic process more than high levels of saturated fats (e.g., beef tallow, coconut oil); diets rich in certain fish oils (e.g., Menhaden oil, Max EPA) are often the most inhibitory to this tumorigenic process. Importantly, however, supplementation of saturated fat or fish oil diets with modest amounts of unsaturated fats, e.g., corn oil, often negates the mammary tumor inhibitory activities of these fats. Thus, rather extreme differences in the types of fat are required for a differential in mammary gland tumorigenesis; common proportionate blends of different fats of animal, plant, and/or fish origin are often unable to differentially influence this tumorigenic process. Diets rich in monoenoic fatty acids, e.g., those containing high levels of olive oil, have been examined in a number of studies; results from these studies have been inconsistent. A number of reports suggest that the increase in development of mammary tumors in rodents fed a high-fat diet, compared with those fed a low-fat diet, is due to specific metabolic activities of the fat per se, activities independent of a caloric mechanism. Careful analysis of these reports suggest that such a conclusion may not be totally warranted. Indeed, persuasive evidence is accumulating indicating that the major mammary tumor development enhancing activities of a high-fat diet may be via a caloric (energy) mechanism. Caloric restriction, even in animals fed a high-fat diet, significantly suppresses mammary tumor development. Even mild caloric restriction (e.g., 12%) can significantly suppress development of mammary tumors in rodents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet.

Stearoyl-coenzyme A desaturase 1-deficient (SCD1(-/-)) mice have impaired MUFA synthesis. When maintained on a very low-fat (VLF) diet, SCD1(-/-) mice developed severe hypercholesterolemia, characterized by an increase in apolipoprotein B (apoB)-containing lipoproteins and the appearance of lipoprotein X. The rate of LDL clearance was decreased in VLF SCD1(-/-) mice relative to VLF SCD1(+/+) mice, indicating that reduced apoB-containing lipoprotein clearance contributed to the hypercholesterolemia. Additionally, HDL-cholesterol was dramatically reduced in these mice. The presence of increased plasma bile acids, bilirubin, and aminotransferases in the VLF SCD1(-/-) mice is indicative of cholestasis. Supplementation of the VLF diet with MUFA- and PUFA-rich canola oil, but not saturated fat-rich hydrogenated coconut oil, prevented these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing LDL-cholesterol, signifying a role for dietary PUFA deficiency in the development of this phenotype. These results indicate that the lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Therefore, endogenous MUFA synthesis is essential during dietary unsaturated fat insufficiency and influences the dietary requirement of PUFA.

Animals↗
PubMed2002

Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease.

Several dietary approaches have reduced cardiovascular events in randomized clinical trials. Replacing saturated fat with polyunsaturated fat prevented coronary events in men, and a Mediterranean diet and fatty fish improved survival. None of these trials had much impact on total fat intake but rather increased vegetable oils, n-3 fatty acids, or many other plant foods or nutrients that are linked to coronary prevention. The reductions in cardiovascular disease (CVD) caused by these dietary therapies compare favorably with drug treatments for hyperlipidemia and hypertension. Improvement in blood lipid risk factors is an important mechanism to explain the results of trials of unsaturated fats. When saturated or trans unsaturated fats are replaced with monounsaturated or n-6 polyunsaturated fats from vegetable oils, primarily low-density lipoprotein (LDL) cholesterol decreases. The LDL to high-density lipoprotein (HDL) cholesterol ratio decreases. When carbohydrates are used to replace saturated fats, in a low-fat diet, LDL and HDL decrease similarly, and the ratio is not improved; triglycerides increase as well when carbohydrate increases, except when low glycemic index foods are used. The n-3 polyunsaturated fats in fish oils suppress cardiac arrhythmias and reduce triglycerides, but they have little effect on LDL or HDL cholesterol levels. The theme should be that diet has benefits that come directly from foods, as well as from the reduction in saturated fats, cholesterol, meats, and fatty dairy foods. It is likely that many diets could be designed that could prevent CVD. This potential diversity is crucial for engaging the diverse cultures and tastes of people worldwide in cardiovascular disease prevention.

Animals↗
PubMed1991

Nutritional factors and pancreatic cancer: a case-control study from south-west Poland.

A population-based case-control study of diet and pancreatic cancer has been conducted in the Opole Voivodeship region in Poland, using 110 cases and 195 controls. A full diet history was used to estimate the daily intake of calories, fat, protein, carbohydrate, cholesterol, retinol, vitamin C, and fibre. There is a strong positive association with the intake of cholesterol with relative risks of 1.90, 3.77, and 4.31 for the 3 upper quartiles compared with the lowest (p, trend = less than 0.01). An inverse association was seen with vitamin C intake, with corresponding relative risks of 1.10, 0.30, and 0.37 (p, trend = less than 0.01). Weak inverse associations were seen with the intake of retinol and fibre. There is evidence of an inverse association with fat intake, particularly unsaturated fats, and of a positive association with the intake of carbohydrate and to a lesser extent, protein. These results further support the potential importance of dietary factors in the aetiology of cancer of the pancreas.

Case-Control Studies↗