Objective: To assess the intake of trans fatty acids (TFA) and other fatty acids in 14 Western European countries. Design and subjects: A maximum of 100 foods per country were sampled and centrally analysed. Each country calculated the intake of individual trans and other fatty acids, clusters of fatty acids and total fat in adults andaor the total population using the best available national food consumption data set. Results: A wide variation was observed in the intake of total fat and (clusters) of fatty acids in absolute amounts. The variation in proportion of energy derived from total fat and from clusters of fatty acids was less. Only in Finland, Italy, Norway and Portugal total fat did provide on average less than 35% of energy intake. Saturated fatty acids (SFA) provided on average between 10% and 19% of total energy intake, with the lowest contribution in most Mediterranean countries. TFA intake ranged from 0.5% (Greece, Italy) to 2.1% (Iceland) of energy intake among men and from 0.8% (Greece) to 1.9% among women (Iceland) (1.2 ± 6.7 gad and 1.7 ± 4.1 gad, respectively). The TFA intake was lowest in Mediterranean countries (0.5 ± 0.8 en%) but was also below 1% of energy in Finland and Germany. Moderate intakes were seen in Belgium, The Netherlands, Norway and UK and highest intake in Iceland. Trans isomers of C 18 X1 were the most TFA in the diet. Monounsaturated fatty acids contributed 9 ± 12% of mean daily energy intake (except for Greece, nearly 18%) and polyunsaturated fatty acids 3 ± 7%. Conclusion: The current intake of TFA in most Western European countries does not appear to be a reason for major concern. In several countries a considerable proportion of energy was derived from SFA. It would therefore be prudent to reduce intake of all cholesterol-raising fatty acids, TFA included.
Several lines of evidence suggest that oxidatively modified low density lipoprotein (LDL) is atherogenic and that antioxidants may protect LDL against oxidation. In addition, cigarette smoking is known to induce oxidant stress. We have examined the effect of ingestion of the antioxidants D,L-ar-tocopherol (vitamin E) and 0-carotene and of smoking on the resistance of LDL against copper-mediated oxidation. Six healthy nonsmoking volunteers ingested 1,000 IU/day D,L-a-tocopherol acetate for 7 days. After vitamin E ingestion concentrations of or-tocopherol in plasma and LDL increased 3.0-and 2.4-fold, respectively. Simultaneously, the oxidation resistance of LDL was elevated significantly (+41%), and the rate of oxidation was decreased significantly (-19%). The increase in o-tocopherol content of LDL and the increase in resistance time were highly correlated (r,=0.89, p=0.014). Eight weeks after termination of the vitamin E intake, o-tocopherol concentrations in plasma and LDL and oxidation resistance of LDL had returned to baseline values. In smokers (n=46), plasma levels of vitamin C (-26%) and concentrations of 0-carotene (-44%, -43%) and total carotenoids (-23%, -29%) in plasma and LDL, respectively, were significantly lower compared with nonsmokers (n=23). No differences were found in o-tocopherol content of LDL and the susceptibility of LDL to lipid peroxidation in both groups. Supplementation of a group of smokers in a 14-week randomized, double-blind, placebo-controlled intervention trial witĥ -carotene resulted in a 16.6-and 5.0-fold increase of LDL /^-carotene and total carotenoid content, respectively. Similar increases were found in plasma without changes in other vitamins. Comparison of the changes in the length of the resistance time between the /J-carotene group (R=23) and the placebo group (n=23) showed no significant differences. We conclude that Ingestion of vitamin E strongly protects LDL against oxidative modification, whereas ^-carotene is not effective, and that smoking does not alter the oxidation resistance of LDL. (Arteriosclerosis and Thrombosis 1992;12:554-562) KEY WORDS • low density lipoprotein oxidation • vitamin E • /3-carotene • cigarette smoking E levated plasma levels of low density lipoprotein (LDL) are associated with an accelerated development of atherosclerotic lesions, which is one of the main causes of coronary artery disease.
This investigation does not support the hypothesis that consumption of black tea protects against four of the major cancers in humans; a cancer-enhancing effect was not evident, either.
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