Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials

https://ir.library.oregonstate.edu/downloads/m326m253d

Importance of n−3 fatty acids in health and disease

Nutrient reference values for Australia and New Zealand: Including recommended dietary intakes

The term Dietary Reference Intakes (DRIs) is new to the field of nutrition. It refers to a set of at least four nutrient-based reference values that can be used for planning and assessing diets and for many other purposes. The development of DRIs replaces the periodic revisions of Recommended Dietary Allowances (RDAs), which have been published since 1941 by the National Academy of Sciences. This is a comprehensive effort being undertaken by the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes of the Food and Nutrition Board, Institute of Medicine, National Academy of Sciences, with the involvement of Health Canada.

Dietary Reference Intakes

Objective: To investigate the effect of a probiotic milk product containing the culture CAUSIDO® and of two alternative products on risk factors for cardiovascular disease in overweight and obese subjects. Design: An 8 week randomized, double-blind, placebo- and compliance-controlled, parallel study. Subjects: Seventy healthy, weight-stable, overweight and obese (25.0<BMI<37.5 kg/m2) males (n=20) and females (n=50), 18–55 y old, were randomly assigned into five groups. Intervention: Four groups consumed 450 ml fermented milk products (yoghurt) daily. Group 1: a yoghurt fermented with two strains of Streptococcus thermophilus and two strains of Lactobacillus acidophilus (StLa). Group 2: a placebo yoghurt fermented with delta-acid-lactone (PY). Group 3: a yoghurt fermented with two strains of Streptococcus thermophilus and one strain of Lactobacillus rhamnosus (StLr). Group 4: a yoghurt fermented with one strain of Enterococcus faecium and two strains of Streptococcus thermophilus (CAUSIDO® culture), GAIO® (G). The dietary composition of the yoghurt was otherwise similar. The fifth group was given two placebo pills (PP) daily. Results: When comparing all five treatment groups, unadjusted for changes in body weight, no statistical effects were observed in week 8 in the G-group on low density lipoproteins (LDL)-cholesterol (P=0.29). After adjustment for small changes in body weight, LDL-cholesterol decreased by 8.4% (0.26±0.10 mmol/l; P<0.05) and fibrinogen increased (0.74±0.32 mmol/l; P<0.05) after 8 weeks in the G-group. This was significantly different from the group consuming chemically fermented yoghurt and the group consuming placebo pills (P<0.05). After 8 weeks, systolic blood pressure was significantly more reduced in the StLa and G-group compared to StLr. No other differences were found. Conclusion: The CAUSIDO® culture reduced LDL-cholesterol and increased fibrinogen in the overweight subjects at a 450 ml consumption daily for 8 weeks. The effect on LDL-cholesterol confirms previous studies. An immunostimulation by one of the strains in the product might explain the effect on fibrinogen in the G-group. Sponsorship: MD Foods A/S, Denmark. European Journal of Clinical Nutrition (2000) 54, 288–297

Effect of 8 week intake of probiotic milk products on risk factors for cardiovascular diseases

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

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 13/4 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 81/2 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.

Effects of Dietary Fat Quality and Quantity on Postprandial Activation of Blood Coagulation Factor VII

Contrary to low-fat meals, high-fat meals are known to cause postprandial factor VII (FVII) activation, but the mechanism is unknown. To study the postprandial FVII activation in detail, 18 young men consumed in randomized order high-fat or low-fat test meals. Fasting and non-fasting blood samples were collected. The high-fat test was associated with an increase in plasma triglyceride and kallikrein concentrations and postprandial FVII activation (p<0.001). Plasma kallikrein was strongly associated with triglycerides in fasting and non-fasting samples (r2=0.74-0.87, p<0.0001), suggesting that triglyceride-rich lipoproteins may activate prokallikrein. Neither plasma triglycerides nor kallikrein and activated FVII were statistically associated. This may suggest that additional factors are involved in the postprandial FVII activation. No clear evidence for a role of tissue factor expression by monocytes, factor XII or insulin in postprandial FVII activation was observed. Tissue factor pathway inhibitor and prothrombin fragment 1+2, a marker of thrombin generation, were not affected postprandially after either the high-fat or the low-fat meals. Our findings indicate that triglyceride-rich lipoproteins activate prokallikrein postprandially, which might form an important initial event in FVII activation after consumption of high-fat meals.

The link between high-fat meals and postprandial activation of blood coagulation factor VII possibly involves kallikrein.

It is a matter of debate whether postprandial activation of blood coagulation factor VII (FVII) is associated with an increased risk of thrombosis. To clarify this question, an animal model in which consequences of dietary FVII activation can be studied in a more detailed way would be an important tool. We studied postprandial FVII activation in seven non-fasting Gottingen minipigs. Intralipid (4 g/kg) was administered through a gastric tube in two fractions at 9.00 a.m. (one-third of total dose) and 10.30 a.m. (two-thirds of total dose). Blood samples were drawn 0.5 h before (baseline) and 2, 3, 3.5, 4, 5, and 6 h after the first fat load. Triglycerides, activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII amidolytic activity (FVIIam) and prothrombin fragment 1 + 2 (F1 + 2) were analysed in plasma samples. Median plasma triglycerides were significantly raised from 0.67 mmol/l l (baseline) to 2.56 mmol/l 5 h postprandially (P< 0.001). There were no significant changes in FVIIa (9.6 U/I at baseline), FVIIam (142% at baseline) and F1 + 2 (0.13 nmol/l at baseline). FVIIc decreased from 141% at baseline to 114% 6 h postprandially (P < 0.001). As a high-fat meal does not seem to activate blood coagulation FVII in minipigs, the pig is apparently not a relevant model for the study of dietary FVII activation and thrombin generation.

A high-fat meal does not activate blood coagulation factor Vii in minipigs

The coagulant activity of blood coagulation factor VII (FVII:C) can be lowered by changes in lifestyle and by therapeutic intervention, e.g. heparin infusion. The question is, however, whether FVII:C determined ex vivo is a valid measure of the FVII activity in vivo. We measured plasma FVII:C, activated FVII (FVIIa), FVII protein (FVII:Ag), tissue factor pathway inhibitor (TFPI), triglycerides, and free fatty acids (FFA) before and 15 min after infusion of a bolus of unfractionated heparin (50 IU/kg body weight) in 12 healthy subjects. Additionally, we conducted in vitro experiments to investigate the effect of unfractionated heparin and TFPI, which is released from the endothelium by heparin, on FVII:C, FVIIa, and FVII:Ag. Heparin infusion decreased triglycerides and increased FFA and TFPI. This was accompanied by significant reductions in FVIIa, FVII:C and FVII:Ag. In vitro, anti-TFPI antibodies increased FVIIa and FVII:C, and heparin reduced FVIIa. The heparinase Hepzyme was unable to abolish the effect of heparin. There were no in vitro effects on FVII:Ag. We conclude that, due to interference by TFPI and heparin in post-heparin plasma, it is impossible to measure the in vivo FVII activity by means of FVII clotting assays. These assays should therefore not be used to measure the coagulation status of patients in heparin therapy, unless extraordinary precautions are taken to eliminate TFPI and heparin effects ex vivo. The observed effect of heparin on FVII:Ag should be investigated further.

In vitro effects of heparin and tissue factor pathway inhibitor on factor VII assays. possible implications for measurements in vivo after heparin therapy.

Lone Frost Larsen

Papers

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

Effects of Dietary Fat Quality and Quantity on Postprandial Activation of Blood Coagulation Factor VII

The link between high-fat meals and postprandial activation of blood coagulation factor VII possibly involves kallikrein.

A high-fat meal does not activate blood coagulation factor Vii in minipigs

In vitro effects of heparin and tissue factor pathway inhibitor on factor VII assays. possible implications for measurements in vivo after heparin therapy.