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The effect on blood pressure of monounsaturated and (n-6)polyunsaturated fatty acids was studied under strict dietary control in normotensive subjects. For 17 days 31 women and 27 men received a control diet providing 19.3% of energy as saturated fat. Then subjects were randomized over two test diets: one diet provided 15.1% of energy from monounsaturated and 7.9% from polyunsaturated fatty acids (‘mono diet’), and the other diet provided 10.8% from monounsaturated and 12.7% from polyunsaturated fatty acids (‘poly diet’). Saturated fat intake was now 12.8% on both diets. Mean blood pressure at the end of the control period was 116/69 mmHg for the mono group and 117/73 mmHg for the poly group. After 5 weeks on the test diet, blood pressure was 115/67 mmHg for the mono group and 117/72 mm Hg for the poly group (difference in changes between the two diet groups was not significant). These findings suggest that at a high fat intake, linoleic acid, when providing more than 7.9% of energy intake, does not influence blood pressure relative to oleic acid in normotensive women and men.

It is well known that saturated fatty acids affect cholesterol metabolism. Relative to carbohydrates, saturated fatty acids increases serum low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol. Of the saturates, lauric and myristic acids have the strongest effects on LDL and HDL cholesterol. Palmitic acid also raises LDL and HDL cholesterol, but less so than lauric and myristic acids do. Stearic acid does not affect LDL and HDL cholesterol. Effects of saturates on platelet aggregation are not consistent. For factor VII activity it appears that lauric, myristic, and palmitic acids have comparable effects, whereas the effects of medium chain fatty acid (MCFA) and stearic acid seem limited.

Effects of monounsaturated fatty acids on serum total cholesterol levels in man are often described as ‘neutral’. The term neutral, however, is often misinterpreted. It does not mean that one can simply add monounsaturates to the diet without changing the serum total cholesterol level but that, under iso-caloric conditions, monounsaturated fatty acids have similar effects on serum total cholesterol as carbohydrates. Diets high in monounsaturated fatty acids, however, have a more favourable effect on the distribution of cholesterol over the various lipoproteins as compared with diets high in carbohydrates. Thus, the term neutral is misleading. In addition, in contrast with earlier studies, recent studies suggest that at realistic intakes, polyunsaturates and monounsaturates have comparable effects on serum lipoprotein levels. At present, there is no unequivocal explanation to resolve this discrepancy. However, these findings offer subjects on cholesterol-lowering diets a larger choice of food items to choose from to replace products high in the serum cholesterol-raising saturated fatty acids.

Studies were performed to investigate the effect of diets rich in oleic or linoleic acids on the activity of plasma cholesteryl ester transfer protein (CETP) in normolipidemic subjects. Previous to the test diets, all subjects consumed a baseline diet rich in saturated fatty acids ("sat-diet") for 17 days. The test diets, rich in either monounsaturated fatty acids ("mono-diet") or rich in polyunsaturated fatty acids ("poly-diet"), were given for 5 weeks to 52 normolipidemic healthy volunteers. The activity of CETP was measured, using a method independent of endogenous plasma lipoproteins, as the rate of exchange of radioactive cholesteryl oleate between labelled LDL and unlabelled HDL. The "mono-diet" induced a statistically significant decrease in CETP activity (from 115 +/- 20 to 102 +/- 19 units/ml plasma, P less than 0.01), while the small decrease on the "poly-diet" (from 111 +/- 23 to 107 +/- 22 units/ml plasma) did not reach significancy. The percentual decrease in CETP activity induced by the "mono-diet" was higher than that induced by the "poly-diet" as was also found for the decrease in LDL cholesterol. In both diet groups a positive correlation was found between changes in CETP activity and changes in plasma total or (VLDL + LDL) cholesterol. The results suggest that high levels of dietary monounsaturated fatty acids may result in decreased plasma CETP activity, as well as LDL cholesterol levels. The mechanisms of these effects, and their possible interrelations, remain to be established.

Objectives. The cholesterol-raising effect of boiled coffee is caused by diterpenes from coffee oil. In order to identify the diterpene responsible, we analysed the diterpene composition of oils from Arabica (Coffea arabica) and Robusta (Coffea canephora robusta) beans and their effects on serum lipids and thyroid function. Design, Subjects, and Intervention. During the first 3-week period of a randomized, cross-over trial, 11 healthy, normolipaemic volunteers received per day either 2 g of coffee oil (n = 5) or placebo oil (n = 6). After a 2-week wash-out, the reverse treatments were applied for another 3 weeks. Six subjects received Arabica oil, supplying 72 mg day -1 cafestol and 53 mg day -1 kahweol, and five received Robusta oil, which provided 40 mg of cafestol, 19 mg of 16-O-methyl-cafestol, and 2 mg of kahweol per day. Background diets were constant. Results. The average serum cholesterol levels rose by 0.65 mmolL-1 (13%) on Arabica oil (P < 0.025 ; 95 % Cl, 0.21-1.09 mmol L -1 ) and by 0.53 mmol L -1 (13%) on Robusta oil (NS ; 95% CI -0.36-1.42 mmmol L -1 . The triglycerides levels rose by 0.54 mmol L -1 (71%) on Arabica (P < 0.005 ; 95% CI, 0.22-0.76 mmol L -1 ) and 0.49 mmol L -1 (61%) on Robusta oil (P

Professor DahlCn’s blank statement that diet has a negligible effect on lipoprotein (a) (Lp(a)) levels [ 1] is correct for conventional lipid-lowering diets, which lower low density lipoprotein (LDL) and sometimes high density lipoprotein (HDL) levels, but hardly affect Lp(a). There is, however, an interesting exception in the form of dietary tram fatty acids, which are unsaturated fatty acids with one or more double bonds in the tram instead of the more usual cis configuration. Intakes in various populations range from l-10 g per day. Three studies in 2 laboratories have shown that tram fatty acids raise Lp(a) in man. Nestel et al. [2] fed 27 mildly hypercholesterolemic men diets enriched with 5%-7% of energy from palmitic acid, oleic acid or tram monounsaturated fatty acids for 3 weeks, and measured Lp(a) by radioimmunoassay. Mean Lp(a) levels (*SD) were 296 f 220 U/l on the

The effects of a high-carbohydrate, high-fiber diet and an olive-oil-rich diet on the distribution of cholesterol over the various lipoproteins, on serum apolipoproteins, and on the composition of HDL2 and HDL3 were studied under strict dietary control. Forty-eight healthy subjects first consumed a high-saturated-fat diet [proportion of energy, en%] (saturated fat 20 en%, total fat 38 en%) for 17 days. For the next 36 days, 24 subjects consumed a diet high in complex carbohydrates (monounsaturated fat 9 en%, total fat 22 en%) and the other 24 consumed a high-fat, olive-oil-rich diet (monounsaturated fat 24 en%, total fat 41 en%). The amounts of protein (12% to 14 en%), polyunsaturated fat (4 to 5 en%), and cholesterol (31 to 35 mg/MJ) were similar in all three diets. Serum cholesterol levels fell by 0.44 mmol/L in subjects consuming the carbohydrate diet and by 0.52 mmol/L for those receiving the olive-oil-rich diet. VLDL-cholesterol levels rose by 0.08 mmol/L in the carbohydrate group and fell by 0.08 mmol/L in the olive oil group (P < .05 for difference between test diets). HDL2 and LDL cholesterol levels fell to the same extent on both diets. HDL3 cholesterol fell by 0.09 mmol/L on the high-carbohydrate diet and increased by 0.01 mmol/L on the olive oil diet (P < .05). There was no change in the composition of HDL3, suggesting that the fall was due to a decrease in the total number of circulating particles. Thus, Keys formula, which predicts no change in serum cholesterol when carbohydrate is replaced by oleic acid, holds for LDL but not for VLDL and HDL, which change in opposite directions. Apolipoprotein (apo) A-I levels decreased by 102 mg/L in the carbohydrate group and rose by 26 mg/L in the olive oil group (P < .05). For apo B these values were 5 mg/L and −83 mg/L, respectively. The apo A-I to apo B ratio decreased by 0.12, or 10%, on the carbohydrate diet and increased by 0.19, or 16%, on the olive oil diet (P < .01). It is concluded that the lipoprotein risk profile for coronary heart disease was affected more favorably by the olive-oil-rich diet than by the diet high in complex carbohydrates.

The effects of two strictly controlled diets, one rich in complex carbohydrates, the other rich in olive oil, on serum lipids were studied in healthy men and women. Serum cholesterol levels fell on average by 0?44 mmol/l in the carbohydrate group and 0?46 mmol/l in the olive oil group. HDL cholesterol levels fell by 0?19 mmol/l in the carbohydrate group and rose by 0?03 mmol/l in the olive oil group. Serum triglycerides rose by 0?19 mmol/l in the carbohydrate group and fell by 0?06 mmol/l in the olive oil group. The changes in both HDL and triglycerides were larger in men than in women. These results clearly show that the olive-oil-rich diet, unlike the complex-carbohydrate-rich diet, caused a specific fall in non-HDL cholesterol while leaving serum triglyceride levels virtually unchanged.

The relation was investigated between body fat topology and serum lipoproteins in healthy, nonobese men and women. Twenty-four men and 24 women consumed a standardized affluent diet for 17 days. Serum was obtained after 14 and 17 days. Regression coefficients of lipids and lipoproteins with age, body mass index, measures of fat distribution, and estimates of fat areas at a cross-section of the body at the level of the umbilicus, were calculated. Waist-to-thigh circumference ratio proved to be the strongest correlate of serum lipids compared with other measures of fat distribution. Upon multiple regression analysis, the waist-to-thigh ratio proved to be a stronger predictor of total cholesterol, LDL-cholesterol and triglyceride levels in men than either age or body mass index. In women this was only true for HDL3-cholesterol. In addition, no significant relations were observed any more of age and body mass index with these serum lipids, with the exception of age for IDL-cholesterol in men. Estimates of intra-abdominal fat area showed in general a stronger correlation with serum lipids than estimates of subcutaneous fat area. It is concluded that, in non-obese subjects, fat distribution is a stronger determinant of serum lipids than either body mass index or age.

Variable amounts of olive oil rather than hard fats were used in classic Mediterranean diets. We review the effects of replacing hard fats with olive oils or starchy foods on blood lipoprotein concentrations. The saturated fatty acids lauric, myristic, and palmitic acids raise both low-density lipoprotein (LDL) and high-density lipoprotein (HDL) somewhat compared with oleic acid. If any fat is replaced by carbohydrates, fasting triglyceride values rise and HDL concentrations fall; effects on LDL depend on the type of fat that is being replaced. Trans isomers of oleic acid lower HDL and raise LDL and lipoprotein(a). The fatty acids in unhydrogenated fish oil potently lower triglycerides but may raise LDL somewhat. When body weight is forcibly kept constant, substitution of unsaturated oils such as olive oil for hard fats rich in saturated or trans fatty acids will produce a more favorable lipoprotein profile than replacement of fat by carbohydrates. However, high-oil diets might lead to obesity, which would undo their favorable effects.

In this thesis we studied the content of acetylsalicylate and total salicylates in foods, and we studied the effects of the dietary non-nutrients salicylates and flavonoids and of certain foods on haemostatic parameters in humans.Acetylsalicylic acid -aspirin- irreversibly inhibits platelet cyclo-oxygenase, leading to decreased platelet thromboxane A 2 production and decreased aggregation. Therefore it is effective as an anti-thrombotic drug in doses as low as 30 mg/d. Qualitative analyses by Swain et al suggested the presence of acetylsalicylate in foods. It was estimated that a normal mixed Western diet provides 10-200 mg/d of total salicylate and 3 mg/d of acetylsalicylate. We showed in 10 healthy subjects that 3 mg/d of acetylsalicylic acid decreased mean platelet thromboxane production by 39±8% (±sd). Thus, quantitative data on dietary acetylsalicylate deserved closer investigation. We determined acetylsalicylate and total salicylates in 30 foods using HPLC with fluorescence detection. Acetylsalicylate was lower than the detection limit (0.02 mg/kg for fresh and 0.2 mg/kg for dried products) in all foods. Total salicylates were 0-1 mg/kg in vegetables and fruits, and 3-28 mg/kg in herbs and spices. We showed that urinary excretion was a valid indicator for intake of pure (acetyl)salicylic acid (recovery 77-80%). We then studied urinary salicylate excretion in 17 subjects eating a variety of diets to estimate the content of bio-available salicylates of diets. Median excretion was 1.4 mg/24 h (range 0.8-1.6). Our data suggest that even purely vegetable diets provide less than 6 mg/d of salicylates, and no measurable acetylsalicylate. These amounts are probably too low to affect coronary heart disease risk, and worries about adverse effects of dietary salicylates on the behaviour of children may be unfounded.Others found that dietary flavonoids were associated with a reduced risk of coronary heart disease and stroke. This might be due to effects on haemostasis, because flavonoids have been reported to inhibit platelet aggregation in vitro . We found that concentrations of 2.5μM of the flavone apigenin inhibited collagen- and ADP-induced platelet aggregation in vitro by about 26%, whereas the flavonols quercetin and quercetin-3-glucoside had no effect. No effects were found on platelet aggregation, thromboxane production, or other haemostatic parameters in 18 healthy subjects after they had consumed large amounts of quercetin- (onions) and apigenin-rich (parsley) foods daily for 7 d each. We conclude that claims for anti-aggregatory effects of flavonoids are based on the in vitro use of concentrations that cannot be attained in vivo . Our findings suggest that it is unlikely that reported effects of dietary flavonoids on coronary vascular disease risk are mediated through platelet aggregation or cyclo-oxygenase activity. Possible effects on known risk indicators for coronary heart disease from the coagulation cascade or the fibrinolytic system should be examined in a larger study.It has been claimed that ginger consumption exerts an anti-thrombotic effect by inhibiting platelet thromboxane production. We, however, found no effects on platelet thromboxane production in a placebo-controlled cross-over study in 18 healthy subjects after consumption of raw (-1±9%, mean±sd) or cooked ginger (1±8%).We conclude that contents of (acetyl)salicylate in foods are too low to affect disease risk. We could not confirm the putative anti-thrombotic effect of ginger, onions and parsley on haemostatic parameters in humans.