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PubMed1996

Dietary fat alters biliary lipid secretion in the hamster.

Dietary fat has been found to alter the incidence of cholesterol gallstones in hamsters: butterfat intensifies while safflower oil reduces lithiasis. WE not report how dietary fat affects bile flow and biliary lipid secretion in this model. Male hamsters were fed one of three experimental diets: a control diet (containing 0.3% cholesterol); control diet + 4.0% butterfat; or control diet + 4.0% safflower oil. After three weeks, bile samples were collected via an external biliary fistula. The endogenous bile acid pool was depleted for 120 min followed by increasing rates of taurocholate infusion for 160 min. Basal secretion of biliary lipids was measured during the bile acid depletion period. Basal bile flow and bile acid output were not significantly different in the three groups. Dietary butterfat increased basal cholesterol output compared to the control diet (0.037 vs. 0.025 mumol/min.kg, respectively); safflower oil did not change cholesterol output (0.027 mumol/min.kg). Hamsters fed butterfat or safflower oil secreted more phospholipid (0.171 and 0.178 mumol/min.kg, respectively) than controls (0.131 mumol/min.kg). The cholesterol/phospholipid output ratio of the butterfat group was higher than the safflower oil group (0.220 vs. 0.153, respectively). Effects of dietary fat on several relationships between file flow and biliary lipid secretion were analyzed by linear regression using the data for the entire bile collection period (bile acid depletion and taurocholate infusion). Butterfat and safflower oil did not change either bile acid dependent or bile acid independent bile flow. Hamsters fed butterfat had a higher linkage coefficient (slope) of cholesterol vs. bile acid output than the safflower oil group (0.023 vs. 0.009, respectively). The linkage coefficient of phospholipid vs. bile acid output of the butterfat group was higher than the controls (0.278 vs. 0.185, respectively). In summary, butterfat induced a high cholesterol and phospholipid secretion with a high cholesterol/phospholipid output ratio; safflower oil induced a high phospholipid secretion with a low cholesterol/phospholipid output ratio. Butterfat and safflower oil have different effects on biliary lipid secretion. These differences in biliary lipid secretion may explain, in part, how butterfat and safflower oil differ in affecting gallstone formation in hamsters.

Animals↗
PubMedDate not supplied

Weight reduction for breast cancer prevention by restriction of dietary fat and calories: rationale, mechanisms and interventions.

A large body of epidemiologic evidence and data drawn from animal feeding studies have led to the feasibility testing of clinical breast cancer prevention trials based on the restriction of dietary fat intake. The animal data strongly suggest that restricting calories as well as fat inhibits breast cancer promotion. Body fat correlates with dietary fat intake in human populations. Obese postmenopausal women have increased levels of circulating bioavailable estrogen capable of promoting breast cancer growth. We propose that restriction of dietary fat intake will decrease total calorie intake and result in a loss of body fat in postmenopausal women. This loss of fat will decrease estrogen production from adrenal androgens and increase bioavailable estrogen, leading to decreased promotion of estrogen-dependent breast tumors. Intervention programs targeted at weight reduction via restriction of calories, reduction of dietary fat and increased physical activity are logical, practical and measurable strategies for reducing the risk of breast cancer in women at moderate to increased risk. Failure to account for variations in adherence to a restricted-fat diet in past feasibility studies has cast doubt on the hypothesis that restricting dietary fat intake can be utilized to reduce the risk of breast cancer. Current studies examining nutritional, hormonal and physiologic data in conjunction with evidence of adherence to dietary and lifestyle change will likely clarify the hormonal and physiologic effects of this potential nutritional strategy for breast cancer prevention.

Animals↗
PubMed2005

The role of dietary fat in obesity.

Current scientific evidence indicates that dietary fat plays a role in weight loss and maintenance. Meta-analyses of intervention trials find that fat-reduced diets cause a 3-4-kg larger weight loss than normal-fat diets. A 10% reduction in dietary fat can cause a 4-5-kg weight loss in individuals with initial body mass index of 30 kg m (-2). Short-term trials show that nonfat dietary components are equally important. Sugar-sweetened beverages promote weight gain, and replacement of energy from fat by sugar-sweetened beverages is counterproductive in diets aimed at weight loss. Protein has been shown to be more satiating than carbohydrate, and fat-reduced diets with a high protein content (20-25% of energy) may increase weight loss significantly. There is little evidence that low-glycemic index foods facilitate weight control. Evidence linking certain fatty acids to body fatness is weak. Monounsaturated fatty acids may even be more fattening than polyunsaturated and saturated fats. No ad libitum dietary intervention study has shown that a normal-fat, high-monounsaturated fatty acid diet is comparable to a low-fat diet in preventing weight gain. Current evidence indicates that the best diet for prevention of weight gain, obesity, type 2 diabetes, and cardiovascular disease is low in fat and sugar-rich beverages and high in carbohydrates, fiber, grains, and protein.

Body Mass Index↗
PubMed2003

Induction of fatal inflammation in LDL receptor and ApoA-I double-knockout mice fed dietary fat and cholesterol.

Atherogenic response to dietary fat and cholesterol challenge was evaluated in mice lacking both the LDL receptor (LDLr(-/-)) and apoA-I (apoA-I(-/-)) gene, LDLr(-/-)/apoA-I(-/-) or double-knockout mice. Gender- and age-matched LDLr(-/-)/apoA-I(-/-) mice were fed a diet consisting of 0.1% cholesterol and 10% palm oil for 16 weeks and compared to LDLr(-/-) mice or single-knockout mice. The LDLr(-/-) mice showed a 6- to 7-fold increase in total plasma cholesterol (TPC) compared to their chow-fed mice counterparts, while LDLr(-/-)/apoA-I(-/-) mice showed only a 2- to 3-fold increase in TPC compared to their chow-fed controls. This differential response to the atherogenic diet was unanticipated, since chow-fed LDLr(-/-) and LDLr(-/-)/apoA-I(-/-) mice began the study with similar LDL levels and differed primarily in their HDL concentration. The 6-fold diet-induced increase in TPC observed in the LDLr(-/-) mice occurred mainly in VLDL/LDL and not in HDL. Mid-study plasma samples taken after 8 weeks of diet feeding showed that LDLr(-/-) mice had TPC concentrations approximately 60% of their 16-week level, while the LDLr(-/-)/apoA-I(-/-) mice had reached 100% of their 16-week TPC concentration after only 8 weeks of diet. Male LDLr(-/-) mice showed similar aortic cholesterol levels to male LDLr(-/-)/apoA-I(-/-) mice despite a 4-fold higher VLDL/LDL concentration in the LDLr(-/-) mice. A direct comparison of the severity of aortic atherosclerosis between female LDLr(-/-) and LDLr(-/-)/apoA-I(-/-) mice was compromised due to the loss of female LDLr(-/-)/apoA-I(-/-) mice between 10 and 14 weeks into the study. Diet-fed female and, with time, male LDLr(-/-)/apoA-I(-/-) mice suffered from severe ulcerated cutaneous xanthomatosis. This condition, combined with a complete depletion of adrenal cholesterol, manifested in fatal wasting of the affected mice. In conclusion, LDLr(-/-) and LDLr(-/-)/apoA-I(-/-) mice showed dramatic TPC differences in response to dietary fat and cholesterol challenge, while despite these differences both genotypes accumulated similar levels of aortic cholesterol.

Adrenal Glands↗
PubMed1999

Dietary fat during pregnancy and lactation increases milk fat and insulin-like growth factor I concentrations and improves neonatal growth rates in swine.

Primiparous (n = 24) and multiparous (n = 24) sows were used to examine the effects of supplemental dietary fat and induction of parturition (d 112) on colostrum and milk composition and suckling piglet growth. Sows were assigned to one of eight treatments on d 90 of gestation that included variables such as parity (1 vs. >/=3), dietary fat (0 vs. 10%), and farrowing (natural vs. induction via lutalyse on d 112). Piglets suckling fat-supplemented dams grew up to 25% faster than control pigs nursing unsupplemented sows (250 vs. 200 g/d; P < 0.01). Improved growth was correlated with elevated milk fat and insulin-like growth factor (IGF) concentrations associated with fat supplementation. Dietary fat elevated milk fat concentration at 48 and 72 h postfarrowing by 21.6 and 22.6%, respectively (P < 0.05). Compared with nonfat-fed controls, multiparous sows fed 10% fat showed a more consistent rise in milk fat concentration, with 26% and 41% elevations for induced or naturally farrowing sows, respectively, vs. a 19% reduction or a 1% elevation in induced or naturally farrowing gilts (P < 0.01). The concentration of milk IGF-I tended to be lower in gilts than in multiparous sows (P < 0.2, 95.7 vs. 117.4 microg/L), and levels were particularly low in milk from induced gilts receiving no additional dietary fat (44.7 microg/L). However, fat supplementation elevated IGF-I to levels (110.6 microg/L) exceeding those measured in unsupplemented, naturally farrowing control sows and gilts (95.8 microg/L). In conclusion, supplemental dietary fat elevates milk fat in multiparous sows more than primiparous gilts regardless of farrowing treatment (induced vs. natural farrowing) and improves piglet growth throughout lactation irrespective of parity or farrowing treatment. The potential of supplemental dietary fat to reverse the reductions in milk IGF-I observed in first-parity females and in dams induced to farrow merits further investigation.

Animals↗
PubMed1997

What do consumers really think about dietary fat?

Nutrition communications in recent years have placed a priority on reducing dietary fat. Survey findings suggest this priority has fostered consumer obsession with and confusion about dietary fat and contributed to misperceptions about healthful eating. The obsession, confusion, and misperceptions about dietary fat and healthful eating, in turn, have created obstacles to achieving dietary goals. This overview of consumer knowledge, attitudes, and behaviors regarding dietary fat may allow dietetics and other professionals to tailor nutrition communication efforts toward clearing the confusion and better fostering success in reaching dietary goals. Nutrition communicators are encouraged to work together to restore reason to nutrition messages and recommendations and joy to food and eating in an effort to help consumers truly achieve nutrition and health goals.

Consumer Behavior↗
PubMed1995

Serum triiodothyronine concentration and Na+,K(+)-ATPase activity in liver and skeletal muscle are influenced by dietary fat type in rats.

It has been shown previously that dietary fat type influences body fat accumulation in rats. The effects of dietary fat type on serum thyroid hormone, activity of Na+,K(+)-ATPase and lipoprotein lipase were studied. Rats were fed an experimental diet containing lard, high oleic safflower oil, safflower oil or linseed oil for 12 wk. Carcass fat content was significantly higher in rats fed the lard diet than in those fed the other diets. However, intra-abdominal adipose tissue weights were not affected by type of dietary fat. The serum triiodothyronine concentration and the activity of Na+,K(+)-ATPase in the liver and skeletal muscle were significantly lower in the lard diet group than in the other diet groups. The lipoprotein lipase activity of abdominal subcutaneous fat was significantly higher in rats fed the lard diet than in rats fed the other diets, but the activity of lipoprotein lipase in intra-abdominal fat was not significantly different. These results suggest that the intake of lard, compared with the intake of the vegetable oils, may decrease Na+,K(+)-ATPase activity in the liver and skeletal muscle by lowering serum triiodothyronine concentration, resulting in the promotion of body fat accumulation.

Adipose Tissue↗
PubMed1997

The role of dietary fat in obesity.

EPIDEMIOLOGY: Epidemiological evidence suggests that a high-fat diet promotes the development of obesity and that there is a direct relationship between the amount of dietary fat and the degree of obesity. The importance of this relationship has been shown in black prepubescent females, who consumed more calories as fat than white females. Moreover, black adult females are heavier and have significant higher cardiovascular disease mortality rates than white females. THE INFLUENCE OF DIETARY FAT ON FOOD INTAKE: An overview of animal studies had indicated that high-fat diets induce greater food intake and weight gain than high-carbohydrate diets. Several factors such as caloric density, satiety properties and post-absorbtive processing can contribute to this different response to high-fat diets. Accordingly, the satiating effects after meals with a high fat:carbohydrate ratio is less than for meals with a lower ratio. Some authors have reported that the most important variable influencing meal size is not the level of hunger but the nutrient content of the range of foods consumed. Thus dietary fat has a weak effect on satiety and we suggest that periodic exposure to a high-fat meal, particularly when hunger is high, may be sufficient to lead to overconsumption of energy as fat in obese patients. DIETARY FAT AND FAT BALANCE: Energy balance is well correlated with fat balance in lean controls, whereas there is no correlation with either carbohydrate or protein balances. Several authors have shown that carbohydrate and protein storage is closely regulated by adjusting oxidation to intake, whereas fat is almost exclusively used or stored in response to day-to-day fluctuations in energy balance. The positive relationship between fat intake and lipid oxidation seen in lean controls appears not to be present in obese patients. On high-fat diets, post-obese women failed to increase the ratio of fat to carbohydrate oxidation appropriately. Increasing dietary fat results in preferential fat storage in post-obese women, impaired suppression of carbohydrate and reduction of 24h energy expenditure. CONCLUSIONS: Dietary fat induces overconsumption and weight gain through its low satiety properties and high caloric density. Obese and post-obese subjects do not appear to adapt to dietary fat, and therefore fat storage is increased.

Adult↗
PubMed2002

Dietary fats, eating guides, and public policy: history, critique, and recommendations.

Controversies over the nutrition science of dietary fat, and equally over the advice furnished to consumers about dietary fat, have confounded US nutrition policies and eating guidance for the last 90 years. This is so despite the remarkable congruence between the first US food guides (1916) and the most recent (2000 Dietary Guidelines for Americans), both of which state that dietary fats should be consumed "moderately." The 2002 Report of the US Food and Nutrition Board (issued jointly by the United States and Canada) quantifies this by stating that healthy dietary fat should constitute "25-35 percent of calories." However, the US consumer guide, the Food Guide Pyramid (released in 1992 but based on data from the early 1980s) states that dietary fats should be consumed "sparingly," which is explained to be "a diet low in fat." This direct conflict in official dietary policies causes consumer confusion and erodes efforts of public and private health promotion efforts to stem the increasing incidence of overweight and obesity in Americans. The most successful population-wide dietary behavior modification program in US history was the food rationing program in World War II. Its successes were based equally on consensus nutrition profiles for good health and messages that communicated the rationing program effectively. The current US incidence of overweight and obesity, and the chronic diseases to which they are precursors, will be mitigated and prevented only with major changes in national dietary policies and programs based on successful experiences and models. The first step in this much-needed process is acknowledgment that current dietary guidance and education policies have been and are unsatisfactory.

Diet, Mediterranean↗
PubMed1998

Effects of the level of dietary fat intake and endurance exercise on plasma cytokines in runners.

PURPOSE: Chronic exercise and high fat diets have been associated with immune suppression. We have reported the effects of level of dietary fat and exercise on lymphocyte subsets, proliferative response, and in vitro production of cytokines by peripheral blood mononuclear cells of runners. The present study was planned to further investigate whether the mechanisms of action of dietary fats is through their modulation of plasma cytokines in runners. METHODS: This study compared plasma cytokines at rest and after endurance exercise at 80% of V02max in female (N = 8-10) and male (N = 8-10) runners after eating diets comprised of 17% (LF), 32% (MF), and 41% (HF) fats (4 wk each). RESULTS: The level of interleukin-1 beta (IL-1 beta) was independent of gender, exercise, and level of dietary fat. tumor necrosis factor (TNF-alpha) level was higher in the plasma of men compared with that in women runners, and the level of these two cytokines increased with increasing level of dietary fat. Plasma interleukin-2 (IL-2) level (a cytokine involved in enhancing T cell functions for host defense) was significantly higher in men compared with that in women runners and decreased in men with increase dietary fat. Plasma interleukin-6(IL-6) level was significantly lower after the endurance run, and IL-6 levels decreased with increase in dietary fat. CONCLUSIONS: Data from the present study suggest that dietary fat has differential effects on plasma cytokine levels in runners. Increasing the level of dietary fat significantly increased endurance run time and had no adverse effects on the level of plasma IL-2 and pro-inflammatory cytokines (IL-1 beta, IL-6 and TNF-alpha in runners.

Adult↗
PubMed1997

Are awareness of dietary fat intake and actual fat consumption associated?--a Dutch-American comparison.

OBJECTIVES: To compare dietary fat intake, the accuracy of individuals' awareness about their fat intake, and sociodemographic and psychosocial correlates of awareness, in Dutch and American samples of employed adults. A discrepancy between objective dietary intake data and subjective self-evaluation of dietary fat consumption has been recognized in the past and might undermine healthy diet promotion interventions, and this is important because people who believe that their diets are healthful are less likely to be interested in making changes. Further, international comparisons have not been examined to date. DESIGN: Data collected for the baseline surveys of the 'Healthy Bergeijk' study in the Netherlands and the 'Working Well Trial' in the United States were compared. SUBJECTS: Working adults from a Dutch community health intervention study (n = 768) and an American worksite health promotion trial (n = 15,440). MAIN OUTCOME MEASURES: Objectively assessed dietary fat intake, measured by food frequency questionnaires, and subjective ratings of fat intake (self-rated fat intake). RESULTS: Findings show that the Dutch respondents had higher objectively assessed fat intake and lower subjective ratings of fat intake (P < 0.001). American respondents perceived their diets as higher in fat, more often stated their intentions to reduce fat intake, and were slightly more likely to make realistic estimates of their dietary fat. Dutch subjects were significantly more likely to underestimate their fat intakes. In both samples, women were most likely to underestimate their fat consumption and the most educated persons were most likely to be realistic. CONCLUSIONS: A substantial proportion of adults, both in the United States and the Netherlands, lack accurate awareness about how much fat they consume, though errors tend to be in opposite directions in the two countries. This study is an important first step toward broadening our international understanding of human dietary behavior for disease prevention.

Adult↗
PubMed1994

Enhancement of the antineoplastic effect of mitomycin C by dietary fat.

In the present study, we investigated the effects of high dietary fat on the growth of MX-1 heterotransplanted in athymic mice and its response to mitomycin C (MC) treatment. We found that high fat intake (25% corn oil, w/w) significantly increased tumor growth, but at the same time it also increased the tumor response to MC treatment compared to the control low fat diet (5% corn oil, w/w). In the tumors from mice fed either low (5% w/w) or high (25% w/w) fat, MC treatment induced oxidative challenge, indicated by significantly increased tumor total superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase peroxidase activities, as well as increased tumor lipid peroxidation. On the other hand, glutathione reductase activity was inhibited by MC treatment. Some of the enzymes which are known to activate MC, such as cytochrome b5 reductase and DT-diaphorase, were also induced in the tumor by high dietary fat intake. The enzyme activities in hepatic tissues were also altered by dietary fat and MC treatment but to a lesser extent. We conclude that high dietary fat intake could enhance the chemotherapeutic effect of MC by increasing MC-activating enzyme activities. The observed increase in lipid peroxidation after MC treatment in MX-1 human mammary carcinoma implanted in the nude mice could result from the observed inhibited glutathione reductase activity. It is tempting to speculate that this might be another antineoplastic mechanism for MC in addition to its known role as a bioreductive alkylating agent. Alternatively, glutathione reductase may be a target for bioreductive alkylation.

Animals↗
PubMed1994

Dietary fat affects plasma prolactin in female F344 rats under conditions of ether stress.

The influence of amount and type of dietary fat on circulating concentrations of prolactin and estradiol-17 beta in female F344 rats from which blood was sampled by decapitation under ether anesthesia was compared with that in rats from which blood was collected without anesthesia. The animals were fed isonutrient (adjusted for differences in energy density) semipurified diets containing 5% or 20% (by weight) sunflower seed oil or lard. Blood was sampled by decapitation with or without standardized ether anesthesia during the afternoon of proestrus-estrus or the morning of metestrus-diestrus, as determined by examination of vaginal smears. Plasma hormone concentrations were measured by radioimmunoassay. Prolactin levels were lower during proestrus-estrus in rats fed a low-fat diet than in animals fed a high-fat diet, statistically independent of the type of dietary fat, but only when blood was sampled by decapitation under ether anesthesia [p = 0.0384, 2-way analysis of variance (ANOVA)]. No such difference was found in rats decapitated without anesthesia. This effect of amount of dietary fat on prolactin in proestrus-estrus animals anesthetized with ether was predominantly present in animals fed polyunsaturated fat (p < 0.05, 1-way ANOVA and Tukey's test) and was statistically not significant in rats fed saturated fat diets. During metestrus-diestrus, prolactin levels were significantly lower in animals fed a high-saturated fat diet than in those fed low-saturated fat, low-unsaturated fat, or high-unsaturated fat diets, independent of the blood sampling conditions (p < 0.05, 2-way ANOVA and Tukey's test). No consistent effects on estradiol-17 beta levels were found in type or amount of dietary fat or in presence or absence of ether anesthesia before decapitation. Growth, apparent digestibility of fat, and caloric intake were similar in all four dietary groups, but food consumption was higher and food conversion efficiency was lower in animals fed low-fat diets than in those fed high-fat diets. This study confirms the hypothesis that effects of dietary fat, particularly polyunsaturated fat, on circulating prolactin occur only during (ether) stress. Because stress is a frequent and normal phenomenon, this observation implies that the mammary glands of animals with a high dietary intake of polyunsaturated fat are frequently exposed to higher circulating prolactin concentrations than rats fed a low-fat diet, which may be a major mechanism by which dietary fat enhances rat mammary carcinogenesis.

Anesthesia, General↗
PubMed1996

Utilization of myristic and palmitic acid in humans fed different dietary fats.

To assess the influence of dietary fat composition on the contribution of dietary myristic and palmitic acid to total fat oxidation and energy production, eight healthy men consumed diets containing 40% of total energy as fat, largely as either butter, tallow or corn oil, for 11 days. On days 8 and 11 of each diet, [1-13C]-myristic or [1-13C]-palmitic acid (20 mg kg-1 body weight) was ingested mixed with the test breakfast meal. Respiratory gas exchange was measured before, and for 9h after, consumption of the meal. Breath 13CO2 enrichments were determined hourly by isotope ratio mass spectrometry. Cumulative 9-h percentage oxidation of dietary myristic acid exceeded that of palmitic acid (P < 0.01), but neither was influenced by fat treatment [n = 8, 7.1% (1.0) (SEM), 8.6% (0.9) and 8.9% (0.6) of dietary myristic acid and 3.3% (0.7), 3.0% (0.9), and 2.5% (0.6) of dietary palmitic acid from butter, tallow and corn oil meals respectively]. Net dietary myristic acid oxidation was greater (P < 0.05) after consumption of the meal high in butter than after consumption of other fats. Net dietary palmitic acid oxidation was similar after consumption of all test meals. Precedent fat treatment had no measurable effect on net fat or carbohydrate oxidation or energy expenditure. The overall contribution of dietary myristic or palmitic acid to total fat oxidation did not exceed 1% over 9 h for any dietary fat. These results suggest that, although dietary fatty acid content is the principal determinant of net dietary fatty acid oxidation, dietary fat sources with moderate differences in fat composition do not measurably alter total energy or substrate utilization after a meal.

Adult↗
PubMed1990

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

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

Adult↗
PubMed1981

Reassessment of the role of dietary fat in cancer etiology.

The role of dietary fat in cancer etiology is briefly discussed in terms of several major types of epidemiological evidence: geographic correlations, migrant studies, low-risk populations, and dietary modification trials. It appears that there is no conclusive evidence that lowering dietary fat intake will result in lowering the cancer death rate. Furthermore, it appears possible to have a relatively low death rate from "diet-related" cancers with an average fat intake. However, in order to fully assess the fat hypothesis, it is important to identify and carefully study a group of Americans with a genuine low-fat diet.

Dietary Fats↗
PubMed2005

Variation in the cholesteryl ester transfer protein (CETP) gene does not influence individual plasma cholesterol response to changes in the nature of dietary fat.

BACKGROUND AND AIMS: Some individuals respond to a greater extent than others to changes in dietary fat and cholesterol even when dietary intake is consistent. A prospective study has been undertaken in which two groups of individuals according to cholesteryl ester transfer protein (CETP) genotype were compared in terms of plasma lipid response to altering the nature of dietary fat in a free-living situation. METHODS AND RESULTS: Following genotyping, 35 individuals with the CETP Taq1 B1B1 genotype were paired with age and sex-matched individuals with one or two CETP B2 alleles, to undertake a single crossover trial with a diet high in saturated fat and a diet high in polyunsaturated fat. There was no washout period between the two 4-week phases. Plasma lipoproteins were measured at the beginning and end of each phase. The difference (95% CI) in plasma LDL-cholesterol concentration at the end of the PUFA and SAFA diets was 0.95 (0.71, 1.19) mmol/l in the CETP B1B1 group and 0.80 (0.57, 1.04) mmol/l in the group with at least one CETP B2 allele. The dietary induced changes in the two genotype groups were not significantly different (p=0.38) from each other. Comparable results were observed for plasma total cholesterol. The high PUFA and SAFA diets did not significantly alter plasma HDL concentration in either of the CETP genotype groups. Response was also similar according to apolipoprotein E genotype (E3E3 vs E4+) and lipoprotein lipase genotype (S447X). CONCLUSIONS: The results of this study do not support previous studies in which CETP genotype predicted plasma LDL-cholesterol response to diet. CETP genotype does not significantly affect the change in plasma total and LDL-cholesterol concentrations that occur when altering the nature of dietary fat. These data suggest that the influence of genetic factors on total and LDL-cholesterol may be relatively small in comparison with the effect of dietary manipulation.

Adult↗