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At least 19 recordsLinked to original sources
PubMed2003

Changes in food sources of dietary fat in response to an intensive low-fat dietary intervention: early results from the Women's Health Initiative.

OBJECTIVE: To evaluate changes in food sources of dietary fat made by participants in the Women's Health Initiative Low-Fat Dietary Modification Trial. DESIGN: This study compares sources of dietary fat intake, estimated by a food frequency questionnaire, between intervention and control participants at baseline, 1 year (year 1) and 2 years (year 2) after randomization. The outcome measure was intake of fat in grams per day. Results are given on consumption of fat from six food groups and the intervention effect, defined as mean change in the intervention group minus the change in controls, controlling for baseline fat intake. PARTICIPANTS: 5,004 intervention and 7,426 control postmenopausal women in 40 clinical centers across the United States. RESULTS: At baseline, the major sources of fat were added fats, such as butter, oils, and salad dressings (25%); meats (21%); and desserts (13%). From baseline to year 1, the intervention group reduced fat by 24.3 g/day compared with the control group. Reductions came primarily from added fats (9.1 g/day), meats (4.6 g/day), and desserts (3.9 g/day). White people reduced added fats more than other race/ethnicity groups did, white and Hispanic people were more likely to reduce fat intake from milk and cheese compared with other groups, and Hispanics reduced fat from mixed dishes more than did other race/ethnicity groups (P<.05 for all). APPLICATIONS/CONCLUSIONS: These data indicate that women in the Women's Health Initiative dietary change intervention made substantial changes in food choices. These results can facilitate future low-fat interventions, and also offer clinical applications, by identifying foods that may be refractory to change.

Black or African American↗
PubMed2000

The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention studies.

The role of high-fat diets in weight gain and obesity has been questioned because of inconsistent reports in the literature concerning the efficacy of ad libitum low-fat diets to reduce body weight. We conducted a meta-analysis of weight loss occurring on ad libitum low-fat diets in intervention trials, and analysed the relationship between initial body weight and weight loss. We selected controlled trials lasting more than 2 months comparing ad libitum low-fat diets with a control group consuming their habitual diet or a medium-fat diet ad libitum published from 1966 to 1998. Data were included from 16 trials with a duration of 2-12 months, involving 1728 individuals. No trials on obese subjects fulfilled the inclusion criteria. The weighted difference in weight loss between intervention and control groups was 2.55 kg (95% CI, 1.5-3.5; P < 0.0001). Weight loss was positively and independently related to pre-treatment body weight (r = 0.52, P < 0.05) and to reduction in the percentage of energy as fat (0.37 kg/%, P < 0.005) in unweighted analysis. Extrapolated to a BMI of about 30 kg/m2 and assuming a 10% reduction in dietary fat, the predicted weight loss would be 4.4 kg (95% CI, 2.0 to -6.8 kg). Because weight loss was not the primary aim in 12 of the 16 studies, it is unlikely that voluntary energy restriction contributed to the weight loss. Although there is no evidence that a high intake of simple sugars contributes to passive overconsumption, carbohydrate foods with a low glycaemic index may be more satiating and exert more beneficial effects on insulin resistance and cardiovascular risk factors. Moreover, an increase in protein content up to 25% of total energy may also contribute to reducing total energy intake. In conclusion, a low-fat diet, high in protein and fibre-rich carbohydrates, mainly from different vegetables, fruits and whole grains, is highly satiating for fewer calories than fatty foods. This diet composition provides good sources of vitamins, minerals, trace elements and fibre, and may have the most beneficial effect on blood lipids and blood-pressure levels. A reduction in dietary fat without restriction of total energy intake prevents weight gain in subjects of normal weight and produces a weight loss in overweight subjects, which is highly relevant for public health.

Body Mass Index↗
PubMed1999

Regulation of gene expression by dietary fat.

Dietary fat is an important macronutrient for the growth and development of all organisms. In addition to its role as an energy source and its effects on membrane lipid composition, dietary fat has profound effects on gene expression, leading to changes in metabolism, growth, and cell differentiation. The effects of dietary fat on gene expression reflect an adaptive response to changes in the quantity and type of fat ingested. Specific fatty acid-regulated transcription factors have been identified in bacteria, amphibians, and mammals. In mammals, these factors include peroxisome proliferator-activated receptors (PPAR alpha, -beta, and -gamma), HNF4 alpha, NF kappa B, and SREBP1c. These factors are regulated by (a) direct binding of fatty acids, fatty acyl-coenzyme A, or oxidized fatty acids; (b) oxidized fatty acid (eicosanoid) regulation of G-protein-linked cell surface receptors and activation of signaling cascades targeting the nucleus; or (c) oxidized fatty acid regulation of intracellular calcium levels, which affect cell signaling cascades targeting the nucleus. At the cellular level, the physiological response to fatty acids will depend on (a) the quantity, chemistry, and duration of the fat ingested; (b) cell-specific fatty acid metabolism (oxidative pathways, kinetics, and competing reactions); (c) cellular abundance of specific nuclear and membrane receptors; and (d) involvement of specific transcription factors in gene expression. These mechanisms are involved in the control of carbohydrate and lipid metabolism, cell differentiation and growth, and cytokine, adhesion molecule, and eicosanoid production. The effects of fatty acids on the genome provide new insight into how dietary fat might play a role in health and disease.

Animals↗
PubMed1988

Phospholipid profile and production of prostanoids by murine colonic epithelium: effect of dietary fat.

Dietary fat and abnormal production of various prostanoids have been linked to various disease states of the large bowel, including cancer of the colon. Studies were conducted to determine the effect of dietary fat (beef tallow or corn oil) on the lipid composition and prostanoid production of the murine colon. Female C57BL/6J mice were fed high-fat (HF) diets (47% of calories as fat) or low-fat (LF) diets (10% of calories as fat). After four wk of dietary treatment, the mucosa was scraped, and lipids were extracted from the mucosal and muscle layers. The fat content of the diets did not significantly alter the amount of phospholipid (PL) or neutral lipid in the colonic tissue. However, the HF affected the PL profile of the colonic mucosa. For example, the ratio of phosphatidylcholine (PC) to phosphatidylethanolamine (PE) was significantly higher for both the HF groups compared with that of the two LF groups (0.76 +/- 0.15 and 0.80 +/- 0.13 vs 0.31 +/- 0.20 and 0.34 +/- 0.18). Production of 13,14-dihydro-15-keto-PGE2 (measured as bicyclic PGE2) and TXB2 (a stable metabolite of TXA2) and PGF1 alpha (a stable metabolite of PGI2) was unaffected by the dietary treatments. The muscle had a different PL profile (PC:PE is 2.6 +/- 0.1) than the mucosa and contributed a larger proportion of the prostanoids formed. This study demonstrates that the phospholipid polar head group composition of normal colonic mucosa is altered by dietary fat, but the ability of the mucosa to synthesize metabolites of PGE2, TXA2 and PGI2 is not affected.

Animals↗
PubMed1984

Dietary modification of fatty acid and prostaglandin synthesis in the rat. Effect of variations in the level of dietary fat.

Dietary supplements with safflower oil, linseed oil, cod liver oil and hydrogenated coconut oil were given to rats at levels of 5, 20 and 40 energy % to simultaneously assess the effects of both type and level of dietary fat on tissue fatty acid composition and prostanoid synthesis. There was no significant change in weight gain or blood pressure between the dietary groups after the 4-week dietary regimen. The liver oil and linseed oil diets depressed the arachidonic acid content of kidney phospholipids at all levels of supplementation. The arachidonic acid content of plasma lipids was significantly elevated in animals on the safflower oil diet at 20 and 40 energy % while those on the same level of liver oil diet showed a marked reduction in arachidonic acid. Whole blood synthesis of thromboxane B2 varied significantly at all levels of fat supplementation, with the 20 energy % safflower oil fed group showing maximally enhanced thromboxane B2 production compared to the coconut oil group (P less than 0.001). Conversely, the liver oil groups showed depressed thromboxane B2 synthesis at 20 and 40 energy % (P less than 0.01) compared to the coconut oil group and at 5 energy % compared to the safflower oil group (P less than 0.05). Production of 6-ketoprostaglandin F1 alpha and prostaglandin E2 by incubated kidney homogenates only differed significantly between the dietary groups at 40 energy %. Urinary excretion of 6-ketoprostaglandin F1 alpha was increased by 45% and 55% in rats fed the safflower oil diet at 20 and 40 energy %, respectively compared to the saturated fat diet, while in the liver oil groups excretion was reduced by 20% and 32%. Dietary suppression of prostanoid synthesis is explained in part by changes in available arachidonic acid and competitive inhibition of cyclooxygenase by (n - 3) fatty acids. Thus, minor changes in dietary fat can readily alter tissue fatty acid composition, but both the extent and nature of changes in phospholipid and prostanoid metabolism vary markedly according to the tissue site.

6-Ketoprostaglandin F1 alpha↗
PubMed1975

Serum cholesterol concentrations and cholelithiasis in rabbits as influenced by the form of dietary fat.

Dietary fats of similar fatty acid composition but in different forms, i.e., olive oil and semipurified oleic acid, were fed to rabbits as 15% of a purified ration for 36 weeks. At periods during the experiment, cholesterol was added to the ration in different amounts. Females rabbits seemed to have greater serum cholesterol concentrations than did male rabbits, and the rabbits fed the oleic acid usually had greater concentrations than did those fed olive oil. After cholesterol was withdrawn from the ration, several weeks were required for the serum cholesterol concentrations to return to pretreatment values. Gallstones and hepatic fatty degeneration were found in rabbits fed either olive oil or oleic acid.

Animal Feed↗
PubMed1987

Effects of fatty acids on gap junctional communication: possible role in tumor promotion by dietary fat.

Dietary lipids, in particular unsaturated fat, promote the development of many experimental tumors. However, no mechanisms to fully explain these effects have been elucidated. Recent reports, which we summarize here, suggest a role for gap junction-mediated intercellular communication in the process of tumor promotion. We also review tumor-promoting effects of dietary fat on experimental, particularly mammary, carcinogenesis. Our main focus is to review recent data examining the inhibitory effects of unsaturated fatty acids on metabolic cooperation in Chinese hamster V79 cells. These data suggest that inhibition of junctional communication may be involved mechanistically in the promotion of tumors by high levels of dietary unsaturated fat. Finally, potential mechanisms by which unsaturated fatty acids inhibit metabolic cooperation are examined.

Animals↗
PubMed1998

Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol.

BACKGROUND: The magnitude of the influence of the apolipoprotein (apo) E genotype on the lipid response to different cholesterol-lowering diet modifications has been controversial. OBJECTIVE: The aim of the study was to investigate the effect of apo E genotype on serum lipid response to the separate modification of dietary fat and cholesterol. DESIGN: A prospective study design with the 3 main apo E genotype groups (3/3, 3/4, and 4/4; n = 15 in each group) was used. Groups were matched for sex, age, body mass index, menopausal status, and baseline serum cholesterol concentration. Subjects followed 3 different diets in fixed order: 1) a standardized baseline diet (38% fat, 300 mg cholesterol/d), 2) a modified National Cholesterol Education Program (NCEP) diet (34% fat, 265 mg cholesterol/d), and 3) the modified NCEP diet + cholesterol (566 mg cholesterol/d). Subjects were middle-aged (50.9 +/- 8.0 y) and mildly hypercholesterolemic (6.55 +/- 1.05 mmol/L). RESULTS: The genotype groups differed in their total cholesterol response to the NCEP diet; the mean (95% CI) decrease being greatest, -14.1% (-19.8%, -8.6% ), in subjects with apo E genotype 4/4 (P = 0.03, analysis of variance). The increase in total cholesterol after addition of 300 mg cholesterol was also greatest in subjects with apo E 4/4 [10.4% (5.8%, 15.1%)] (P = 0.03, analysis of variance). CONCLUSIONS: Apo E genotype modified the lipid response to changes in both dietary fat and cholesterol in mildly hypercholesterolemic subjects; the response was greatest in subjects with apo E genotype 4/4 and even a moderate increase in dietary cholesterol resulted in a 10% elevation in serum total cholesterol in them.

Adult↗
PubMed1997

A randomized trial of a low-fat dietary intervention in women at high risk for breast cancer.

A randomized intervention trial of dietary fat reduction to 15% of total calories was initiated in 1987 for women at high risk for breast cancer to determine the feasibility of recruiting and maintaining them on a low-fat diet. The study has enrolled 194 women between the ages of 18 and 67 years who met at least one of three eligibility criteria: 1) a first-degree relative with breast cancer, 2) a P2 or DY Wolfe mammographic pattern, and 3) a prior breast biopsy demonstrating epithelial hyperplasia with or without atypia. Eligible women must also have had diets that contained > or = 30% of calories from fat at entry. Women were randomized to a nonintervention usual diet vs. a 15% low-fat diet. Recruitment was sought through physicians, personal mailings, breast cancer patients, and the news media. Two study sites participated: a large urban hospital affiliated with a university medical center and a community oncology private practice. The results from both institutions were similar and demonstrated that a low-fat dietary plan could be effectively conducted in private as well as academic settings with recruitment tailored to the community where the trial is being conducted. Reduction in dietary fat intake was maximal during the first three months of the dietary intervention and remained stable throughout 12 months of follow-up. Reductions in total calories, weight loss, and percent body fat were minimal. The nonintervention group experienced no major change in their diet. We conclude that it is feasible to recruit women who are at high risk for breast cancer into a dietary intervention trial and with sufficient dietary counseling and motivation on the part of participants, reduction in dietary fat intake can be achieved and maintained. More in-depth analyses of these data will be presented in subsequent reports.

Adolescent↗
PubMed1997

Fat preferences, dietary fat intake and body composition in children.

OBJECTIVE: To examine the relationship between fat preference, dietary intake data and body composition in children. SUBJECT AND METHODS: Subjects studied were 88 children aged 9-12 y from two elementary schools in Ohio. Measures for dietary intake and body composition were obtained by 3 day diet records, anthropometrics, triceps and subscapular skinfolds. Fat preference data was assessed by hedonic rating of high and low fat snack foods. RESULTS: Data indicate that children who preferred the high fat snack items had high dietary fat intakes (r = 0.57, P < 0.05). Tricep skinfold measurement and BMI correlated positively with high fat food preferences (r = 0.51 and r = 0.46 P < 0.05). CONCLUSIONS: These data suggest preference for high fat foods may occur due to diet composition and that increased adiposity may be associated with higher relative fat intakes.

Body Composition↗
PubMed1992

No effect of adult dietary fat on tumors induced prenatally by diethylstilbestrol.

Strain CD-1 female mice exposed prenatally to diethylstilbestrol (DES) or vehicle were placed on semipurified diets containing 2.6%, 10%, 20%, or 29% fat by weight at four weeks of age. These mice were used as a breeding colony for a few weeks and then maintained to terminal illness on the semipurified diets. Females exposed prenatally to DES developed mammary tumors, pituitary tumors, and glandular tumors of the reproductive tract. There was no significant difference in tumor frequency between low- and high-fat dietary groups. Fewer tumors appeared in the vehicle-exposed mice, as expected, and their frequency did not differ between the dietary groups. Pregnancy reduced tumor frequency in DES-exposed mice, but the incidence of pregnancy was not significantly different between low- and high-fat dietary groups. In the adult the failure of a high-fat diet to increase the frequency of reproductive system tumors induced prenatally is in marked contrast to the effectiveness of high-fat diets in promoting mammary tumors induced by carcinogens given to rats postnatally. This difference is critical in the interpretation of epidemiological studies. The relationship of dietary fat to reproductive system cancer in human populations was reviewed in comparison with these two animal models. The epidemiological literature was found to be more consistent with the animal model, showing high sensitivity to dietary fat prenatally but no significant sensitivity at the adult stage of life.

Animals↗
PubMed1983

Dietary factors in colon carcinogenesis with special emphasis on the role of dietary fat and dietary fibre.

Dietary factors other than fat and fibre have been reported to influence colon cancer risk, in particular a protective effect of cruciferous vegetables (Graham et al., 1978) and an increased risk associated with beer consumption (Breslow and Enstrom, 1974) have been suggested. The role of these dietary aspects is however less well understood than that of fat and fibre; for beer consumption the statistical association has been suggested to be a non-causal nature (Jensen, 1979; Jensen, 1982). In summary then the epidemiological pattern of colon cancer points to various aspects of diet as a determinant of colon cancer risk. If - as suggested - an imbalance between the intake of fat and fibre is of importance mediated by the fecal concentration of bile acids further studies should attempt to clarify the relative role of these two items in addition to shedding further light on the role of other dietary aspects, for which our present knowledge is even more incomplete. With a view to cancer prevention it may prove more productive to give priority to a search for items that have a protective effect. It may thus be more acceptable to high risk populations to add perhaps only a limited amount of "roughage" to their diets than to reduce the daily fat-intake.

Colonic Neoplasms↗