Association between Butter, Margarine, and Olive Oil Intake and Asthma Symptoms among School Children: Result from a Large-Scale Cross-Sectional Study.

Background: There are conflicting results about the association between dietary fat intake and asthma symptoms. Since few studies in the Middle East have been explored the relation between dietary fat consumption and risk of asthma, the present study was conducted to investigate the association between the consumption of butter, margarine, and olive oil and asthma risk in school children living in central Iran. Method: In this cross-sectional study, out of 10,240 participants, asthma and its symptoms and dietary intake of butter, margarine, and olive oil of 7,667 children and adolescents were assessed using a validated International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire. The relationship between fat subtypes and asthma was assessed using logistic regression. Results: The prevalence of asthma confirmed by a doctor in the study population was 4.22%. An inverse association was found between butter and margarine consumption once or twice a week and odds of current asthma and wheezing in the past 12 months (OR = 0.52, 95% CI: 0.28-0.96; OR = 0.7, 95% CI: 0.55-0.88, respectively); however, those with higher consumption did not have a higher chance for developing wheezing or asthma. Conclusion: We found that margarine and butter intake one or two times a week might have an inverse association with asthma and its symptoms among children. Prospective cohort studies are recommended to confirm these findings.

The association between dairy intake and risk of cardiovascular disease and mortality in patients with stable angina pectoris.

AIMS: The association of dairy products with cardiovascular disease and mortality risk remains heavily debated. We aimed to investigate the association between intake of total dairy and dairy products and the risk of acute myocardial infarction (AMI), stroke, and cardiovascular and all-cause mortality. METHODS AND RESULTS: We included 1929 patients (80% men, mean age 62 years) with stable angina pectoris from the Western Norway B-vitamin Intervention Trial. Dietary data were obtained via a 169-item food frequency questionnaire. Risk associations were estimated using Cox proportional hazard regression models adjusted for relevant covariates. Non-linear associations were explored visually. The mean (±SD) dairy intake in the study population was 169 ± 108 g/1000 kcal. Median follow-up times were 5.2, 7.8, and 14.1 years for stroke, AMI, and mortality, respectively. Higher intake of total dairy and milk were positively associated with stroke risk [HR (95% CI): 1.14 (1.02, 1.27) and 1.13 (1.02, 1.27), cardiovascular mortality 1.06 (1.00, 1.12) and 1.07 (1.01, 1.13)] and all-cause mortality [1.07 (1.03, 1.11) and 1.06 (1.03, 1.10)] per 50 g/1000 kcal. Higher cheese intake was inversely associated with AMI risk [0.92 (0.83, 1.02)] per 10 g/1000 kcal. Butter was associated with increased AMI risk [1.10 (0.97, 1.24)] and all-cause mortality [1.10 (1.00, 1.20) per 5 g/1000 kcal. CONCLUSION: Higher dairy and milk consumption were associated with increased risk of mortality and stroke. Cheese was associated with decreased, and butter with increased, risk of AMI. Dairy is a heterogenous food group with divergent health effects and dairy products should therefore be investigated individually.

Fortifying Butterfat with Soybean Oil Attenuates the Onset of Diet-Induced Non-Alcoholic Steatohepatitis and Glucose Intolerance.

The addition of plant oils such as soybean oil (S) to a diet rich in saturated fatty acids is discussed as a possible route to prevent or diminish the development of metabolic disease. Here, we assessed whether a butterfat-rich diet fortified with S affects the development of early non-alcoholic steatohepatitis (NASH) and glucose intolerance. Female C57BL/6J mice were fed a standard-control diet (C); a fat-, fructose-, and cholesterol-rich diet (FFC, 25E% butterfat, 50% (wt./wt.) fructose, 0.16% (wt./wt.) cholesterol); or FFC supplemented with S (FFC + S, 21E% butterfat + 4E% S) for 13 weeks. Indicators of liver damage, inflammation, intestinal barrier function, and glucose metabolism were measured. Lipopolysaccharide (LPS)-challenged J774A.1 cells were incubated with linolenic and linoleic acids (ratio 1:7.1, equivalent to S). The development of early NASH and glucose intolerance was significantly attenuated in FFC + S-fed mice compared to FFC-fed mice associated with lower hepatic toll-like receptor-4 mRNA expression, while markers of intestinal barrier function were significantly higher than in C-fed mice. Linolenic and linoleic acid significantly attenuated LPS-induced formation of reactive nitrogen species and interleukin-1 beta mRNA expression in J774A.1 cells. Our results indicate that fortifying butterfat with S may attenuate the development of NASH and glucose intolerance in mice.

Fortifying diet with rapeseed oil instead of butterfat attenuates the progression of diet-induced non-alcoholic fatty liver disease (NAFLD) and impairment of glucose tolerance.

BACKGROUND: Absolute dietary fat intake but even more so fatty acid pattern is discussed to be critical in the development of non-alcoholic fatty liver disease (NAFLD). Here, we determined if switching a butterfat enriched diet to a rapeseed oil (RO) enriched diet affects progression of an existing NAFLD and glucose intolerance in mice. METHODS: For eight weeks, female C57Bl/6J mice were either fed a liquid control (C) or a butterfat-, fructose- and cholesterol-rich diet (BFC, 25E% butterfat) to induce early signs of steatohepatitis and glucose intolerance in mice. For additional five weeks mice received either BFC or C or a fat-, fructose- and cholesterol-rich and control diet, in which butterfat was replaced with RO (ROFC and CRO). Markers of glucose metabolism, liver damage and intestinal barrier were assessed. RESULTS: Exchanging butterfat with RO attenuated the progression of BFC diet-induced NAFLD and glucose intolerance. Beneficial effects of RO were associated with lower portal endotoxin levels and an attenuation of the induction of the toll-like receptor-4-dependent signaling cascades in liver. Peroxisome proliferator-activated receptor γ activity was induced in small intestine of ROFC-fed mice. CONCLUSION: Taken together, exchanging butterfat with RO attenuated the progression of diet-induced steatohepatitis and glucose intolerance in mice.

Dairy Products and Cancer Risk in a Northern Sweden Population.

The role of dairy products in cancer is unclear. We assessed consumption of fermented milk, non-fermented milk, cheese, and butter, estimated from semi-quantitative food frequency questionnaires, in relation to prospective risk of breast, prostate, colorectal, smoking-, and obesity-related cancers in 101,235 subjects, including 12,552 cancer cases, in the population-based Northern Sweden Health and Disease Study. Most analyses (n = 20) rendered null results. In men, we observed an increased prostate cancer risk among high-consumers of cheese (hazard ratio (HR) for highest vs. lowest quintile (Q5-Q1), 1.11; 95% CI, 0.97-1.27; Ptrend = 0.013). In women, high-consumers of cheese had a decreased risk of overall cancer (HR Q5-Q1, 0.95; 95% CI, 0.88-1.04; Ptrend = 0.039), smoking-related (HR Q5-Q1, 0.84; 95% CI, 0.72-0.97; Ptrend ≤ 0.001), and colorectal cancers (HR Q5-Q1, 0.82; 95% CI, 0.63-1.07; Ptrend = 0.048). Butter yielded a weak decreased obesity-related cancer risk in women (HR Q5-Q1, 0.91; 95% CI, 0.81-1.02; Ptrend = 0.049). Fermented milk yielded HRs below zero in women, but with no clear linear associations. In conclusion, this study does not support any major adverse or beneficial effects of fermented milk, non-fermented milk, cheese, and butter in the diet from a cancer risk perspective.

On Meat, Butter, and Fudge.

Was the Annals of Internal Medicine recently acting as a mouthpiece for meat-industry propaganda? Five papers underpinned recommendations on meat consumption; their central deceit was to review only randomized controlled trials and cohort studies, which, in research on the associations between common foods and disease outcomes, are nearer to the bottom than the top of the evidence hierarchy. Despite concluding that their own recommendations were "weak and based on low certainty evidence", the authors were happy to recommend that there is "No need to reduce red or processed meat consumption for good health." What we actually know is that: red meat consumption is an order of magnitude higher now than through most of human history; red meat is a probable, and processed meat is a definite, human carcinogen; saturated fat increases risk of heart disease; and vegans and vegetarians have better lipid profiles, lower risk of chronic disease, and greater longevity than meat eaters. There are other consequences of meat consumption too, including: altered sexual development; widespread antimicrobial resistance; and disrupted planetary health, including depletion of aquifers, groundwater pollution, and increased greenhouse gases. The pseudoscience presented in the Annals of Internal Medicine appears to have been written solely to create doubt and confusion in the wider population. Scientists and journals should hold themselves to a higher standard.

Saturated Fats from Butter but Not from Cheese Increase HDL-Mediated Cholesterol Efflux Capacity from J774 Macrophages in Men and Women with Abdominal Obesity.

Background: Recent evidence suggests that the association between dietary saturated fatty acids (SFAs) and coronary artery disease risk varies according to food sources. How SFAs from butter and cheese influence HDL-mediated cholesterol efflux capacity (CEC), a key process in reverse cholesterol transport, is currently unknown. Objective: In a predefined secondary analysis of a previously published trial, we have examined how diets rich in SFAs from either cheese or butter influence HDL-mediated CEC, compared with diets rich in either monounsaturated fatty acids (MUFAs) or polyunsaturated fatty acids (PUFAs). Methods: In a randomized crossover controlled consumption trial, 46 men and women with abdominal obesity consumed 5 isocaloric diets, each for 4 wk. Two diets were rich in SFAs either from cheese (CHEESE) or butter (BUTTER) [12.4-12.6% of energy (%E) as SFAs, 32%E as fat, 52%E as carbohydrates]. In 2 other diets, SFAs (5.8%E) were replaced with either MUFAs from refined olive oil (MUFA) or PUFAs from corn oil (PUFA). Finally, a lower fat and carbohydrate diet was used as a control (5.8%E as SFAs, 25.0%E as fat, 59%E as carbohydrates; CHO). Post-diet HDL-mediated CEC was determined ex vivo using radiolabelled J774 macrophages incubated with apolipoprotein B-depleted serum from the participants. Results: Mean (±SD) age was 41.4 ± 14.2 y, and waist circumference was 107.6 ± 11.5 cm in men and 94.3 ± 12.4 cm in women. BUTTER and MUFA increased HDL-mediated CEC compared with CHEESE (+4.3%, P = 0.026 and +4.7%, P = 0.031, respectively). Exploring the significant diet × sex interaction (P = 0.044) revealed that the increase in HDL-mediated CEC after BUTTER compared with CHEESE was significant among men (+6.0%, P = 0.047) but not women (+2.9%, P = 0.19), whereas the increase after MUFA compared with CHEESE was significant among women (+9.1%, P = 0.008) but not men (-0.6%, P = 0.99). Conclusion: These results provide evidence of a food matrix effect modulating the impact of dairy SFAs on HDL-mediated CEC with potential sex-related differences that deserve further investigation. This trial was registered at clinicaltrials.gov as NCT02106208.

Randomised trial of coconut oil, olive oil or butter on blood lipids and other cardiovascular risk factors in healthy men and women.

INTRODUCTION: High dietary saturated fat intake is associated with higher blood concentrations of low-density lipoprotein cholesterol (LDL-C), an established risk factor for coronary heart disease. However, there is increasing interest in whether various dietary oils or fats with different fatty acid profiles such as extra virgin coconut oil may have different metabolic effects but trials have reported inconsistent results. We aimed to compare changes in blood lipid profile, weight, fat distribution and metabolic markers after four weeks consumption of 50 g daily of one of three different dietary fats, extra virgin coconut oil, butter or extra virgin olive oil, in healthy men and women in the general population. DESIGN: Randomised clinical trial conducted over June and July 2017. SETTING: General community in Cambridgeshire, UK. PARTICIPANTS: Volunteer adults were recruited by the British Broadcasting Corporation through their websites. Eligibility criteria were men and women aged 50-75 years, with no known history of cancer, cardiovascular disease or diabetes, not on lipid lowering medication, no contraindications to a high-fat diet and willingness to be randomised to consume one of the three dietary fats for 4 weeks. Of 160 individuals initially expressing an interest and assessed for eligibility, 96 were randomised to one of three interventions; 2 individuals subsequently withdrew and 94 men and women attended a baseline assessment. Their mean age was 60 years, 67% were women and 98% were European Caucasian. Of these, 91 men and women attended a follow-up assessment 4 weeks later. INTERVENTION: Participants were randomised to extra virgin coconut oil, extra virgin olive oil or unsalted butter and asked to consume 50 g daily of one of these fats for 4 weeks, which they could incorporate into their usual diet or consume as a supplement. MAIN OUTCOMES AND MEASURES: The primary outcome was change in serum LDL-C; secondary outcomes were change in total and high-density lipoprotein cholesterol (TC and HDL-C), TC/HDL-C ratio and non-HDL-C; change in weight, body mass index (BMI), waist circumference, per cent body fat, systolic and diastolic blood pressure, fasting plasma glucose and C reactive protein. RESULTS: LDL-C concentrations were significantly increased on butter compared with coconut oil (+0.42, 95% CI 0.19 to 0.65 mmol/L, P<0.0001) and with olive oil (+0.38, 95% CI 0.16 to 0.60 mmol/L, P<0.0001), with no differences in change of LDL-C in coconut oil compared with olive oil (-0.04, 95% CI -0.27 to 0.19 mmol/L, P=0.74). Coconut oil significantly increased HDL-C compared with butter (+0.18, 95% CI 0.06 to 0.30 mmol/L) or olive oil (+0.16, 95% CI 0.03 to 0.28 mmol/L). Butter significantly increased TC/HDL-C ratio and non-HDL-C compared with coconut oil but coconut oil did not significantly differ from olive oil for TC/HDL-C and non-HDL-C. There were no significant differences in changes in weight, BMI, central adiposity, fasting blood glucose, systolic or diastolic blood pressure among any of the three intervention groups. CONCLUSIONS AND RELEVANCE: Two different dietary fats (butter and coconut oil) which are predominantly saturated fats, appear to have different effects on blood lipids compared with olive oil, a predominantly monounsaturated fat with coconut oil more comparable to olive oil with respect to LDL-C. The effects of different dietary fats on lipid profiles, metabolic markers and health outcomes may vary not just according to the general classification of their main component fatty acids as saturated or unsaturated but possibly according to different profiles in individual fatty acids, processing methods as well as the foods in which they are consumed or dietary patterns. These findings do not alter current dietary recommendations to reduce saturated fat intake in general but highlight the need for further elucidation of the more nuanced relationships between different dietary fats and health. TRIAL REGISTRATION NUMBER: NCT03105947; Results.

Nonfermented milk and other dairy products: associations with all-cause mortality.

Background: A positive association between nonfermented milk intake and increased all-cause mortality was recently reported, but overall, the association between dairy intake and mortality is inconclusive.Objective: We studied associations between intake of dairy products and all-cause mortality with an emphasis on nonfermented milk and fat content.Design: A total of 103,256 adult participants (women: 51.0%) from Northern Sweden were included (7121 deaths; mean follow-up: 13.7 y). Associations between all-cause mortality and reported intakes of nonfermented milk (total or by fat content), fermented milk, cheese, and butter were tested with the use of Cox proportional hazards models that were adjusted for age, sex, body mass index, smoking status, education, energy intake, examination year, and physical activity. To circumvent confounding, Mendelian randomization was applied in a subsample via the lactase LCT-13910 C/T single nucleotide polymorphism that is associated with lactose tolerance and milk intake.Results: High consumers of nonfermented milk (≥2.5 times/d) had a 32% increased hazard (HR: 1.32; 95% CI: 1.18, 1.48) for all-cause mortality compared with that of subjects who consumed milk ≤1 time/wk. The corresponding value for butter was 11% (HR: 1.11; 95% CI: 1.07, 1.21). All nonfermented milk-fat types were independently associated with increased HRs, but compared with full-fat milk, HRs were lower in consumers of medium- and low-fat milk. Fermented milk intake (HR: 0.90; 95% CI: 0.86, 0.94) and cheese intake (HR: 0.93; 95% CI: 0.91, 0.96) were negatively associated with mortality. Results were slightly attenuated by lifestyle adjustments but were robust in sensitivity analyses. Mortality was not significantly associated with the LCT-13910 C/T genotype in the smaller subsample. The amount and type of milk intake was associated with lifestyle variables.Conclusions: In the present Swedish cohort study, intakes of nonfermented milk and butter are associated with higher all-cause mortality, and fermented milk and cheese intakes are associated with lower all-cause mortality. Residual confounding by lifestyle cannot be excluded, and Mendelian randomization needs to be examined in a larger sample.

Long-term exposure to a butter-rich diet induces mild-to-moderate steatosis in Chang liver cells and Swiss albino mice models.

BACKGROUND: Butter is one of the widely used fats present in the diet. However, there is no satisfactory study available that evaluates the effect of a high-fat diet containing butter as the principal fat on the development of non-alcoholic fatty liver disease (NAFLD). METHODS: In the present study, butter was used for the development of steatosis in Chang liver cells in an in vitro study and Swiss albino mice in an in vivo study. In vitro steatosis was established, and butter was compared with oleic acid in Chang liver cells using an oil red O (ORO)-based colorimetric assay. In the in vivo study, a butter-rich special diet was fed for 15 weeks to mice, who showed no significant change in body weight. The expression pattern of phosphatase and tensin homolog (PTEN) and miR-21 was compared by reverse transcriptase-PCR. RESULTS AND CONCLUSIONS: Special diet-fed animals showed downregulated PTEN compared to normal diet-fed animals, while levels of miR-21 remained the same. Elevations in biochemical parameters, viz., triglycerides and liver function tests showed symptoms of onset of NAFLD. Histophathological study of livers of test animals confirmed mild-to-moderate degree of NAFLD.

Newspaper debates on milk fats and vegetable oils in Finland, 1978-2013: An analysis of conflicts over risks, expertise, evidence and pleasure.

The study analysed public debates on the association of milk fats, vegetable oils and cardiovascular diseases (CVDs) between 1978 and 2013 in Finland, a country with a decades-long history of public health initiatives targeting fat consumption. The main agendas, conflicts and participants were analysed. The data were collected from the newspaper Helsingin Sanomat and consisted of 52 threads and 250 texts. We identified four themes around which there were repeated, often overlapping conflicts: the health risks of saturated fats, expertise of the risks of fat consumption, the adequate evidence of the risks of fat consumption, and framing the fat question. During the research period, the main arguments of the effects of consumption of fats have remained the same. References to epidemiological and intervention studies and framing of the fat question as a public health issue, have been ongoing, as has the definition of what constitutes genuine expertise. Yet, we also found discontinuities. In the early 2000s new emphases began to emerge: personal experiences were increasingly presented as evidence of the effects of dietary choices on human health, and the question of fat consumption was framed either as one of enjoyment or of a consumers' right to choose rather than only being a public health question. Moreover, new professional groups such as chefs and creative professionals now joined the discussion.

Efficacy of phytosterols and fish-oil supplemented high-oleic-sunflower oil rich diets in hypercholesterolemic growing rats.

Phytosterols (P) and fish-oil (F) efficacy on high-oleic-sunflower oil (HOSO) diets were assessed in hypercholesterolemic growing rats. Controls (C) received a standard diet for 8 weeks; experimental rats were fed an atherogenic diet (AT) for 3 weeks, thereafter were divided into four groups fed for 5 weeks a monounsaturated fatty acid diet (MUFA) containing either: extra virgin olive oil (OO), HOSO or HOSO supplemented with P or F. The diets did not alter body weight or growth. HOSO-P and HOSO-F rats showed reduced total cholesterol (T-chol), non-high-density lipoprotein-cholesterol (non-HDL-chol) and triglycerides and increased HDL-chol levels, comparably to the OO rats. Total body fat (%) was similar among all rats; but HOSO-F showed the lowest intestinal, epididymal and perirenal fat. However, bone mineral content and density, and bone yield stress and modulus of elasticity were unchanged. Growing hypercholesterolemic rats fed HOSO with P or F improved serum lipids and fat distribution, but did not influence material bone quality.

Is the metabolic syndrome inversely associates with butter, non-hydrogenated- and hydrogenated-vegetable oils consumption: Tehran lipid and glucose study.

AIM: The aim of this study was to investigate the association between hydrogenated- (HVOs) and non-hydrogenated vegetable oils (non-HVOs) and butter and the metabolic syndrome (MetS) after 3-years of follow-up in adults. METHODS: This study was conducted between 2006-2008 and 2009-2011 within the framework of the Tehran Lipid and Glucose Study, on 1582 adults, aged 19-84 years. Intakes of HVOs, non-HVOs and butter were assessed by a validated semi-quantitative food frequency questionnaire. Based on the consumption of food rich in fat including HVOs, non-HVOs and butter, participants were categorized to consumers and non-consumers. RESULTS: Of 1582 participants during a 3-year follow-up, 15.2% developed MetS. Non-consumption of butter was associated with lower MetS risk compared with its consumption. Among consumers of food rich in fat, intake of HVOs and butter were associated with an increased risk of MetS; ORs in the final multivariate model were 2.70 (95% CI: 1.52-4.78) for HVOs and 2.03 (95% CI: 1.20-3.41) for butter, in the highest, compared to the lowest category of dietary intakes. Intake of non-HVOs was not associated with risk of MetS. CONCLUSIONS: Consumption of HVOs and butter were positively associated with an increase risk of MetS.

[The oleic triglycerides of palm oil and palmitic triglycerides of creamy fat. The reaction of palmitoylation, potassium and magnesium palmitate, absorption of fatty acids by enterocytes and microbiota of large intestine].

The decreasing of content of animal, palmitic milk fat (butter) by means of its substitution with vegetable, oleic, palmy oil in food of adults optimal by its quantity is physically chemically and biologically substantiated. In oleic palmy oil higher content of oleic mono unsaturated fatty acid and oleic triglycerides than in creamy fat is established. The biologic availability of palmitic unsaturated palmitic acid in the form of free fatty acid is decreased at its absorption by enterocytes of small intestines is detected. There are no transforms of mono unsaturated acids in palmy oil in contrast with hydrogenated margarines. In palmy, oleic oil there is not enough of short-chained fatty acids (C4-C6) and it has no taste quality and it has low level of unsaturated fatty acids and factually it is lacking of ω-6 polyunsaturated fatty acids. However, it is compensated in case of availability offish and sea products in food. If adults, especially older ones, will refuse to consume creamy fat and decrease intake of products with high content of palmitic unsaturated fatty acid and palmitic triglycerides (beef, sour cream, fatty cheeses) it'll positively impact their health. The refusal from these products is a real step in prevention of metabolic pandemic (atherosclerosis and atheromatosis, metabolic syndrome, resistance to insulin, obesity). There are still large number of people who at optimal amount of food retain in vivo increased amount of exogenous, endogenously synthesized from glucose palmitic unsaturated fatty acid in the form of unesterified fatty acids (syndrome of resistance to insulin) and increased content of palmitic triglycerides.

Feeding butter with elevated content of trans-10, cis-12 conjugated linoleic acid to obese-prone rats impairs glucose and insulin tolerance.

BACKGROUND: We recently demonstrated that feeding a natural CLAt10,c12-enriched butter to lean female rats resulted in small, but significant increases in fasting glucose and insulin concentrations, and impaired insulin tolerance. Our goal was to extend these findings by utilizing the diabetes-prone female fatty Zucker rat. Rats were fed custom diets containing 45 % kcal of fat derived from control and CLAt10,c12-enriched butter for 8 weeks. METHODS: CLA t10,c12-enriched butter was prepared from milk collected from cows fed a high fermentable carbohydrate diet to create subacute rumen acidosis (SARA); control (non-SARA) butter was collected from cows fed a low grain diet. Female fatty Zucker rats (10 weeks old) were randomly assigned to one of four diet treatments: i) low fat (10 % kcal), ii) 45 % kcal lard, iii) 45 % kcal SARA butter, or iv) 45 % kcal non-SARA butter. A low fat fed lean Zucker group was used as a control group. After 8 weeks, i) glucose and insulin tolerance tests, ii) insulin signaling in muscle, adipose and liver, and iii) metabolic caging measurements were performed. RESULTS: Glucose and insulin tolerance were significantly impaired in all fatty Zucker groups, but to the greatest extent in the LARD and SARA conditions. Insulin signaling (AKT phosphorylation) was impaired in muscle, visceral (perigonadal) adipose tissue and liver in fatty Zucker rats, but was generally similar across dietary groups. Physical activity, oxygen consumption, food intake and weight gain were also similar amongst the various fatty Zucker groups. CONCLUSIONS: Increasing the consumption of a food naturally enriched with CLAt10,c12 significantly worsens glucose and insulin tolerance in a diabetes-prone rodent model. This outcome is not explained by changes in tissue insulin signaling, physical activity, energy expenditure, food intake or body mass.

Butter increased total and LDL cholesterol compared with olive oil but resulted in higher HDL cholesterol compared with a habitual diet.

BACKGROUND: Butter is known to have a cholesterol-raising effect and, therefore, has often been included as a negative control in dietary studies, whereas the effect of moderate butter intake has not been elucidated to our knowledge. OBJECTIVE: We compared the effects of moderate butter intake, moderate olive oil intake, and a habitual diet on blood lipids, high-sensitivity C-reactive protein (hsCRP), glucose, and insulin. DESIGN: The study was a controlled, double-blinded, randomized 2 × 5-wk crossover dietary intervention study with a 14-d run-in period during which subjects consumed their habitual diets. The study included 47 healthy men and women (mean ± SD total cholesterol: 5.22 ± 0.90 mmol/L) who substituted a part of their habitual diets with 4.5% of energy from butter or refined olive oil. RESULTS: Study subjects were 70% women with a mean age and body mass index (in kg/m²) of 40.4 y and 23.5, respectively. Butter intake increased total cholesterol and LDL cholesterol more than did olive oil intake (P < 0.05) and the run-in period (P < 0.005 and P < 0.05, respectively) and increased HDL cholesterol compared with the run-in period (P < 0.05). No difference in effects was observed for triacylglycerol, hsCRP, insulin, and glucose concentrations. The intake of saturated fatty acids was significantly higher in the butter period than in the olive oil and run-in periods (P < 0.0001). CONCLUSIONS: Moderate intake of butter resulted in increases in total cholesterol and LDL cholesterol compared with the effects of olive oil intake and a habitual diet (run-in period). Furthermore, moderate butter intake was also followed by an increase in HDL cholesterol compared with the habitual diet. We conclude that hypercholesterolemic people should keep their consumption of butter to a minimum, whereas moderate butter intake may be considered part of the diet in the normocholesterolemic population.

Olive oil consumption and risk of type 2 diabetes in US women.

BACKGROUND: Olive oil has been shown to improve various cardiometabolic risk factors. However, to our knowledge, the association between olive oil intake and type 2 diabetes (T2D) has never been evaluated in the US population. OBJECTIVE: We aimed to examine the association between olive oil intake and incident T2D. DESIGN: We followed 59,930 women aged 37-65 y from the Nurses' Health Study (NHS) and 85,157 women aged 26-45 y from the NHS II who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by validated food-frequency questionnaires, and data were updated every 4 y. Incident cases of T2D were identified through self-report and confirmed by supplementary questionnaires. RESULTS: After 22 y of follow-up, we documented 5738 and 3914 incident cases of T2D in the NHS and NHS II, respectively. With the use of Cox regression models with repeated measurements of diet and multivariate adjustment for major lifestyle and dietary factors, the pooled HR (95% CI) of T2D in those who consumed >1 tablespoon (>8 g) of total olive oil per day compared with those who never consumed olive oil was 0.90 (0.82, 0.99). The corresponding HRs (95% CIs) were 0.95 (0.87, 1.04) for salad dressing olive oil and 0.85 (0.74, 0.98) for olive oil added to food or bread. We estimated that substituting olive oil (8 g/d) for stick margarine, butter, or mayonnaise was associated with 5%, 8%, and 15% lower risk of T2D, respectively, in the pooled analysis of both cohorts. CONCLUSIONS: Our results suggest that higher olive oil intake is associated with modestly lower risk of T2D in women and that hypothetically substituting other types of fats and salad dressings (stick margarine, butter, and mayonnaise) with olive oil is inversely associated with T2D.

Impact of the consumption of a rich diet in butter and it replacement for a rich diet in extra virgin olive oil on anthropometric, metabolic and lipid profile in postmenopausal women.

OBJECTIVE: To analyze the impact of the substitution of a rich diet in saturated fats with a rich diet in monounsaturated fats on anthropometric, metabolic and lipid profile in postmenopausal women. MATERIAL AND METHODS: A prospective, longitudinal and comparative study where 18 postmenopausal women participated in two periods of dietary intervention of 28 days each one: 1) (SAT diet) consumed butter. Caloric formula (CF) = 15% protein, 38% fat. [20% saturated fat (SFA), 12% monounsaturated fat (MUFA) and 47% carbohydrates and 6% polyunsaturated (PUFA)]. b) Period MONO: with extra virgin olive oil (EVOO). CF = 15% protein, 38% fat (<10% SFA, 22% PUFA and 6% MUFA) and 47% carbohydrates. Size and body composition, glucose, insulin, HOMA, TC, HDL-C, LDL-C, VLDL-C, TG, TC/HDL-C, LDL-C/HDL-C, TG/HDL-C and non-HDL-C/HDL.C were measured; dietary Anamnesis/24 hours, daily food record. ANOVA and Bonferroni statistical analysis (SPSS 20) was applied. RESULTS: The age was 56 ± 5 years, BMI 29.8 ± 3.1 kg/m2, waist circumference: 93.2 ± 10.1 cm, waist/hip ratio: 0.86 ± 0.14, waist/height: 0.59 ± 0.06 and 38.6 ± 4% body fat (NS). Lipid profile: SAT diet increased TC (p <0.001), LDL-C (p <0.002) and non HDL-Cholesterol (p <0.000), HDL-C increased in MONO diet (p <0.000). SAT diet: TC/HDL-c ratio, Non col HDL-c/HDL-c, LDL-c/HDL-c (p <0.000) and TG/HDL-c (p <0.000). In MONO diet decreased TC/HDL-c (p <0.015) and TG/HDL-c (p <0.016). CONCLUSIONS: The SAT diet increased cardiovascular risk, while the MONO diet decreased the risk to develop the metabolic syndrome components and choronary heart disease.

Objetivo: analizar el impacto de la sustitución de una dieta rica en grasas saturadas por una dieta rica en grasas monoinsaturadas sobre el perfil antropométrico, metabólico y lipídico en mujeres postmenopáusicas. Material y método: estudio prospectivo, longitudinal y comparativo en el que 18 mujeres postmenopáusicas participaron en dos períodos de intervención dietética de 28 días cada uno: 1) (dieta SAT) consumieron mantequilla. Fórmula calórica (FC) = 15% de proteínas, 38% grasas. [20% grasas saturadas (AGS), 12% grasas monoinsaturadas (AGM) y 47% carbohidratos y 6% poliinsaturadas (AGPI)]. 2) Periodo MONO: con aceite de oliva virgen extra (AOVE). Fórmula calórica = 15% de proteínas, 38% grasas (.