Replacing dairy fat with rapeseed oil causes rapid improvement of hyperlipidaemia: a randomized controlled study.

BACKGROUND: Rapeseed oil (RO), also known as canola oil, principally contains the unsaturated fatty acids 18:1n-9, 18:2n-6 and 18:3n-3 and may promote cardiometabolic health. OBJECTIVE: To investigate the effects on lipoprotein profile, factors of coagulation and insulin sensitivity of replacing a diet rich in saturated fat from dairy foods (DF diet) with a diet including RO-based fat (RO diet). DESIGN: During a 2×3-week randomized, controlled, cross-over trial, 20 free-living hyperlipidaemic subjects were provided with isocaloric test diets that differed in fat composition alone. Blood lipoprotein profile, coagulation and fibrinolytic factors and insulin sensitivity (euglycaemic clamp) were determined before and after the dietary intervention. RESULTS: All subjects completed the study, and compliance was high according to changes in serum fatty acids. The RO diet, but not the DF diet, reduced the levels of serum cholesterol (-17%), triglycerides (-20%) and low-density lipoprotein cholesterol (-17%), cholesterol/high-density lipoprotein (HDL) cholesterol ratio (-21%), apolipoprotein (apo) B/apo A-I ratio (-4%) and factor VII coagulant activity (FVIIc) (-5%) from baseline. These changes were significantly different between the diets (P=0.05 to P<0.0001), except for FVIIc (P=0.1). The RO diet, but not the DF diet, modestly increased serum lipoprotein(a) (+6%) and tended to increase the glucose disappearance rate (K-value, +33%). HDL cholesterol, insulin sensitivity, fibrinogen and tissue plasminogen activator inhibitor-1 levels did not change from baseline or differ between the two diets. CONCLUSIONS: In a diet moderately high in total fat, replacing dairy fat with RO causes a rapid and clinically relevant improvement in serum lipoprotein profile including lowering of triglycerides in hyperlipidaemic individuals.

Fish oil feeding is associated with an increased accumulation of dietary lipids in enterocytes: results from an in vivo study in rats.

BACKGROUND: Chronic fish oil consumption is associated with reduced postprandial lipaemia, but the mechanism behind this effect is not fully understood. We studied whether lipid absorption might be altered in rats fed fish oil. METHODS: Male Wistar rats were fed fish oil enriched chow (n = 6) or control oil enriched chow (n = 6). After 4 weeks, 61 mg 3H-triolein was instilled into duodenal tied-off loops. Intestinal segments were removed after 15, 30, 45, 60 and 90 min. Enterocytes were then isolated by calcium chelation and quantified by DNA determination. Non-absorbed 3H-lipid and 3H-lipid contents of enterocytes were determined by liquid scintillation counting. Two other groups of rats (2 x 6) fed the experimental diets were given an oral fat load and fasting and postprandial blood samples were taken. RESULTS: The accumulation of 3H-lipids in enterocytes was higher in rats fed fish oil than in controls (area under the 3H-lipid time curve: 1041.3 versus 670.3 nmol oleic acid x min/microg DNA, P < 0.05). Separation of lipids showed that an accumulation of triglycerides and free fatty acids occurred in rats fed fish oil. The amount of non-absorbed 3H-lipid tended to be higher in the fish oil fed rats (P > 0.1). It was confirmed that the fish oil enriched chow caused lower postprandial lipaemia (34% reduction in serum triglyceride concentrations, P < 0.05). CONCLUSION: Attenuated postprandial lipaemia following fish oil feeding is explained, at least partly, by a transient lipid accumulation in enterocytes which may result in a delayed triglyceride efflux from the enterocytes into the circulation.

Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes.

OBJECTIVE: Fish oil supplement has been proposed as a non-pharmacological strategy to correct the atherogenic lipid profile associated with type 2 diabetes mellitus. However, fish oil may have deleterious effects on lipid peroxidation and glycemic control. DESIGN: In this study, 44 type 2 diabetic patients were randomized to vitamin E standardized (53.6 mg/day) supplementation (capsules) with 4 g daily of either fish oil (n=23) or corn oil (n=21) for 8 weeks preceded by a 4 week run-in period of corn oil supplementation. LDL was isolated by density gradient ultracentrifugation and oxidized in vitro with Cu(2+). As a marker of in vivo oxidation malondialdehyde concentration in LDL (LDL-MDA) was measured. RESULTS: Fish oil reduced both mean lag time (before, 57.8; after, 48.8 min, P<0.001) and mean propagation rate (before, 0.018 DeltaOD/min; after, 0.015 DeltaOD/min, P<0.001), whereas corn oil had no influence on lag time and propagation rate. The changes in lag time and propagation rate differed significantly between fish oil and corn oil treatment. LDL-MDA changes differed borderline significantly between groups (FO, 110.4 pmol/mg protein; CO, 6.7 pmol/mg protein; P=0.057). Fish oil supplementation had no influence on glycemic control as assessed from HbA(1c) and fasting blood glucose. CONCLUSION: According to our findings, fish oil supplementation leads to increased in vivo oxidation and increased in vitro oxidation susceptibility of LDL particles. More studies are needed to clarify the clinical importance of this finding.

The Göttingen minipig as a model for postprandial hyperlipidaemia in man: experimental observations.

Postprandial hyperlipidaemia is believed to be atherogenic. This study aimed to establish a minipig model to investigate determinants of postprandial lipid metabolism. In a randomized cross-over design seven minipigs were subjected to six different feeding regimens: intragastric fat loads of 1, 2, and 4 g fat (Intralipid, 20%) kg(-1) in two fractions 1.5 h apart (1/3 first, 2/3 second), 2 g fat (Intralipid kg(-1) in one fraction, and 2 g olive oil kg(-1) in two fractions, all after pre-feeding with standard diet, and finally 2 g fat (Intralipid kg(-1) in two fractions without pre-feeding. Blood was sampled before and hourly for 7 h after gavaging, and plasma triglycerides were measured. Triglycerides increased significantly in all the feeding regimens (P < 0.001), except when olive oil was used as the fat source. A borderline significant dose-response effect of the Intralipid dose on the triglyceride response was observed. We found no significant differences in triglyceride response whether 2 g fat (Intralipid kg(-1) was given in one or two fractions, with or without pre-feeding. We conclude that postprandial hyperlipidaemia in minipigs can be induced by gavaging an emulgated lipid solution (1-4 g fat/kg, Intralipid, while olive oil is not applicable. There is no need to administer the fat fractionated or to withhold food prior to administration.

[The effect of dietary oils on blood lipids and the risk of ischemic heart disease with special emphasis on olive oil. A literature review]. / Spiseoliers effekt på blodlipider og risiko for iskaemisk hjertesygdom med saerlig fokus på olivenolie. En litteraturgennemgang.

INTRODUCTION: The European Union is financing a large-scale campaign, in which olive oil is represented as the optimal fat for dietetic prevention of coronary heart disease. METHOD: We reviewed all controlled dietary studies comparing the effect on blood lipids of olive oil and alternative vegetable oils. Fifteen studies were identified. RESULTS: Consumption of olive oil was associated with significantly raised plasma concentrations of low density lipoprotein cholesterol (+6.5%), high density lipoprotein cholesterol (), and triglycerides (+7%) as compared with an average of the alternative oils. In the light of these differences in blood lipids and the risk coefficients published earlier, we calculated that the consumption of olive oil was associated with a 7% increase in the risk of coronary heart disease. CONCLUSION: We conclude that olive oil cannot be considered more cardioprotective than other unsaturated vegetable oils as judged from its effects on blood lipids.

An olive oil-rich diet results in higher concentrations of LDL cholesterol and a higher number of LDL subfraction particles than rapeseed oil and sunflower oil diets.

We investigated the effect of olive oil, rapeseed oil, and sunflower oil on blood lipids and lipoproteins including number and lipid composition of lipoprotein subclasses. Eighteen young, healthy men participated in a double-blinded randomized cross-over study (3-week intervention period) with 50 g of oil per 10 MJ incorporated into a constant diet. Plasma cholesterol, triacylglycerol, apolipoprotein B, and very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) cholesterol concentrations were 10;-20% higher after consumption of the olive oil diet compared with the rapeseed oil and sunflower oil diets [analysis of variance (ANOVA), P < 0.05]. The size of IDL, VLDL, and LDL subfractions did not differ between the diets, whereas a significantly higher number (apolipoprotein B concentration) and lipid content of the larger and medium-sized LDL subfractions were observed after the olive oil diet compared with the rapeseed oil and sunflower oil diets (ANOVA, P < 0.05). Total HDL cholesterol concentration did not differ significantly, but HDL(2a) cholesterol was higher after olive oil and rapeseed oil compared with sunflower oil (ANOVA, P < 0.05).In conclusion, rapeseed oil and sunflower oil had more favorable effects on blood lipids and plasma apolipoproteins as well as on the number and lipid content of LDL subfractions compared with olive oil. Some of the differences may be attributed to differences in the squalene and phytosterol contents of the oils.

Effect of meal fat quality on oxidation resistance of postprandial VLDL and LDL particles and plasma triacylglycerol level.

This study was performed to examine the postprandial effects of meals containing dietary fats, with their natural fatty acid composition and tocopherol content, on the plasma triacylglycerols (TG) and tocopherols and on the resistance of VLDL and LDL to oxidation. On six separate days eighteen healthy male subjects were given low-fat meals (LF) or the LF meals enriched with sunflower oil (SO), rapeseed oil (RO), olive oil (OO), palm oil (PO), or butter (B) in a crossover design. The fat-rich meals all resulted in similar postprandial TG responses while the LF test meal did not increase plasma TG level. The postprandial plasma fatty acid profile changed to resemble the fatty acid composition of the ingested test fat. The alpha-tocopherol:gamma-tocopherol ratios in postprandial plasma and VLDL samples were greater than in the test fats. We found that the resistance of VLDL particles to oxidation in the postprandial state as assessed from lag time was increased after the PO-rich meal as compared with the SO-rich meal (p = 0.018), and the propagation rate was greater after the SO- and RO-rich meals compared with the others (p < 0.001). The resistance of LDL particles to oxidation was unaffected by the meals. In postprandial VLDL samples, the content of alpha-tocopherol was greater after the OO- and SO-rich meals compared with the meal rich in PO (P = 0.034 and 0.042 respectively). The gamma-tocopherol content of VLDL was highest after RO-meal as compared with all other test meals (P = 0.0019), and higher after SO as compared with B (P = 0.0148). Large individual differences were noted. In conclusion, meals enriched with different fats lead to the formation of VLDL particles with varying resistance to oxidation.

Are olive oil diets antithrombotic? Diets enriched with olive, rapeseed, or sunflower oil affect postprandial factor VII differently.

BACKGROUND: The incidence of ischemic heart disease (IHD) in Crete was lower than expected on the basis of blood lipid concentrations of participants in the Seven Countries Study. A favorable effect of a high intake of olive oil on thrombogenesis may have contributed to this finding. OBJECTIVE: We compared the effects of virgin olive oil with those of rapeseed and sunflower oils on blood coagulation factor VII (FVII), a key factor in thrombogenesis. DESIGN: In a randomized and strictly controlled crossover study, 18 healthy young men consumed diets enriched with 5 g/MJ (19% of total energy) olive oil, sunflower oil, or rapeseed oil for periods of 3 wk. On the final day of each period, participants consumed standardized high-fat meals (42% of energy as fat). Fasting and nonfasting blood samples were collected after each period. RESULTS: Mean (+/-SEM) nonfasting peak concentrations of activated FVII (FVIIa) were 11.3 +/- 5.1 U/L lower after olive oil than after sunflower oil, an 18% reduction (P < 0.05). Olive oil also tended to cause lower FVIIa peak concentrations than did rapeseed oil (mean difference: 8.6 U/L, a 15% reduction; P = 0.09). There were no significant differences between diets with respect to nonfasting factor VII coagulant activity (FVII:c), prothrombin fragment 1+2 (F1+2), and tissue factor pathway inhibitor (TFPI) concentrations, or with respect to fasting plasma values of FVII protein, FVII:c, FVIIa, F1+2, or TFPI. CONCLUSION: A background diet rich in olive oil may attenuate the acute procoagulant effects of fatty meals, which might contribute to the low incidence of IHD in Mediterranean areas.

Fish consumption and coronary heart disease mortality. A systematic review of prospective cohort studies.

OBJECTIVES: To review all prospective cohort studies examining the relationship between fish intake and coronary heart disease mortality, and to assess the strength and consistency of their findings. DESIGN: Systematic review of studies based on individual records of fish or n-3 polyunsaturated fatty acid consumption and coronary heart disease death. Studies were given scientific quality scores and divided into categories of high, intermediate, or insufficient quality. MAIN OUTCOME MEASURE: Coronary heart disease mortality. RESULTS: Eleven studies were identified. The cohorts counted a total of 116764 individuals. Of four studies judged to be of high quality, the two largest (n = 44895 and 20051) were performed in populations at low risk of coronary heart disease. They found no protective effect of fish consumption. The other two high-quality studies were relatively small (n = 852 and 1822) and included individuals at higher risk. They both found an inverse relationship between fish consumption and coronary heart disease death, suggesting that 40-60 g fish per day is optimal and associated with a risk reduction of 40-60%. Results of four studies of intermediate quality support that fish consumption is inversely associated with coronary heart disease mortality in high-risk populations only. Three studies were judged to be of insufficient quality to be used for drawing conclusions. CONCLUSIONS: Fish consumption is not associated with reduced coronary heart disease mortality in low-risk populations. However, fish consumption at 40-60 g daily is associated with markedly reduced coronary heart disease mortality in high-risk populations. The underlying biochemical mechanism is not known and causal inference premature.

Postprandial lipoprotein, glucose and insulin responses after two consecutive meals containing rapeseed oil, sunflower oil or palm oil with or without glucose at the first meal.

There is increasing evidence that the degree of postprandial lipaemia may be of importance in the development of atherosclerosis and IHD. Postprandial lipid, lipoprotein, glucose, insulin and non-esterified fatty acid (NEFA) concentrations were investigated in eleven healthy young males after randomized ingestion of meals containing rapeseed oil, sunflower oil or palm oil with or without a glucose drink. On six occasions each subject consumed consecutive meals (separated by 1.75 h) containing 70 g (15 g and 55 g respectively) of each oil. On one occasion with each oil 50 g glucose was taken with the first meal. One fasting and fifteen postprandial blood samples were taken over 9 h. There were no statistically significant differences in lipoprotein and apolipoprotein responses after rapeseed, sunflower and palm oils, whereas insulin responses were lower after sunflower oil than after rapeseed oil (ANOVA, P = 0.04). The NEFA and triacylglycerol concentrations at 1.5 h were reduced when 50 g glucose was taken with the first meal (ANOVA, P < 0.0001 and P < 0.05 respectively), regardless of meal fatty acid composition. In conclusion, the consumption of glucose with a mixed meal containing either rapeseed, sunflower or palm oil influenced the immediate triacylglycerol and NEFA responses compared with the same meal without glucose, whereas no significant effect on postprandial lipaemia after a subsequent meal was observed. The fatty acid composition of the meal did not significantly affect the lipid and lipoprotein responses, whereas an effect on insulin responses was observed.

Effects of dietary fat quality and quantity on postprandial activation of blood coagulation factor VII.

Acute elevation of the coagulant activity of blood coagulation factor VII (FVIIc) is observed after consumption of high-fat meals. This elevation is caused by an increase in the concentration of activated FVII (FVIIa). In a randomized crossover study, we investigated whether saturated, monounsaturated, or polyunsaturated fats differed regarding postprandial activation of FVII. Eighteen healthy young men participated in the study. On 6 separate days each participant consumed two meals (times, 0 and 1 3/4 hours) enriched with 70 g (15 and 55 g) of either rapeseed oil, olive oil, sunflower oil, palm oil, or butter (42% of energy from fat) or isoenergetic low-fat meals (6% of energy from fat). Fasting and series of nonfasting blood samples (the last at time 8 1/2 hours) were collected. Plasma triglycerides, FVIIc, FVIIa, and free fatty acids were analyzed. There were marked effects of the fat quantity on postprandial responses of plasma triglycerides, FVII, and free fatty acids. The high-fat meals caused, in contrast to the low-fat meals, considerable increases in plasma triglycerides. Plasma levels of FVIIc and FVIIa peaks were 7% and 60% higher after consumption of high-fat meals than after consumption of low-fat meals. The five different fat qualities caused similar postprandial increases in plasma triglycerides, FVIIc, and FVIIa. These findings indicate that high-fat meals may be prothrombotic, irrespective of their fatty acid composition. The postprandial FVII activation was not associated with the plasma triglyceride or free fatty acid responses.

Dietary fish oil (4 g daily) and cardiovascular risk markers in healthy men.

Some epidemiological observations indicate that 1 to 2 weekly servings of fish prevent ischemic heart disease (IHD). This might be explained by an effect of the very-long-chain n-3 polyunsaturated fatty acids (n-3 VLCPUFA) of fish oil on lipid metabolism and/or the hemostatic system, both involved in IHD development. We studied the effect of incorporating natural fish oil (4 g daily equivalent to 0.91 g n-3 VLCPUFA and corresponding to one to two weekly servings of fatty fish) into the diet in a 4-week parallel, randomized, and double-blind trial of 47 healthy males aged 29 to 60 years. Sunflower oil was used as placebo. The fish oil had no significant effect on plasma lipids, apolipoproteins, lipoprotein(a), blood coagulation FVII, fibrinogen, endogenous fibrinolysis, beta-thromboglobulin, von Willebrand factor, glucose, or insulin in fasting blood samples. In nonfasting samples (n = 19), fish oil was associated with an approximately 30% decline in plasma triglycerides (P < .02) and a 9% decline in FVII protein (P < .05), whereas FVII coagulant activity and fibrinolysis were unaffected. In conclusion, our findings indicate that lowering of postprandial triglycerides is the only n-3 VLCPUFA effect that could contribute to primary prevention of IHD in healthy middle-aged men as assessed by currently measurable lipid and hemostatic risk markers.

[Should I also eat fish oils? A critical assessment of the use of fish oils in the prevention of ischemic heart disease]. / Bør jeg også spise fiskeolier? En kritisk vurdering af fiskeolier i forebyggelsen af iskoemisk hjertesygdom.

The effect of a daily dietary supplement of 6 g fish oil (3.4 g eicosapentaenoic and docosahexaenoic acid) on body weight, blood pressure, bleeding time and blood lipids was assessed in an open trial. The fish oil was taken for four weeks by nine 30-55 year-old individuals. An age- and sex-matched control group took equivalent amounts of safflower oil, which has an overall fatty acid composition similar to the tested fish oil. The fish oil supplement caused significant changes in body weight (median: +0.9 kg), systolic blood pressure (-10 mmHg), diastolic blood pressure (-5 mmHg), and high density lipoprotein (HDL) cholesterol concentration (+0.21 mmol/l), whereas serum triglycerides decreased insignificantly (-0.25 mmol/l). Low density lipoprotein (LDL) concentration were not affected. We observed no changes in the control group. In the discussion, it is underlined that fish oil supplementation may affect some risk markers of ischemic heart disease favourably. However, other important risk markers, including LDL cholesterol, are unaffected or unfavourably affected by fish oils. A more uni-directional reduction in risk can be attained by a change in dietary habits, which should be preferable to a fish oil supplement in the general population. Individuals who show critically low HDL/total cholesterol ratios, who are hypertriglyceridemic, or are mildly hypertensive may, however, benefit from a fish oil supplement of the amount tested here.

Nutritional status and mortality of patients in regular dialysis therapy.

The relationship between mortality and nutritional status of 48 chronic dialysis patients (32 patients on haemodialysis (HD) and 16 on continuous ambulatory peritoneal dialysis (CAPD)) was studied over a 24-month period. Patients were scored individually according to relative body weight (RBW), S-transferrin, mid-arm muscle circumference (MAMC) and triceps skinfold thickness (TSF), and were given a total score from 0 (normal nutritional status) to 8 (severe protein-caloric malnutrition) at start of observation. The observation period was characterized by a significantly lower total nutritional score among surviving (n = 39) patients than among patients who died (n = 9) (Mann-Whitney, P less than 0.001). There was no difference in mortality between the two kinds of dialysis therapy (HD,CAPD). In conclusion, chronic dialysis patients with a poor nutritional status have a highly increased mortality. The presumably causal nature of this relationship makes prevention of protein-caloric malnutrition among dialysis patients a high priority task.