Dietary phenols are antioxidants, and their consumption might contribute to the prevention of cardiovascular disease. Coffee and tea are major dietary sources of phenols. Dietary phenols are metabolized extensively in the body. Lack of quantitative data on their metabolites hinders a proper evaluation of the potential biological effects of dietary phenols in vivo. The aim of this study was to identify and quantify the phenolic acid metabolites of chlorogenic acid (major phenol in coffee), quercetin-3-rutinoside (major flavonol in tea) and black tea phenols in humans, and determine the site of metabolism. Healthy humans (n = 20) with an intact colon participated in a dietary controlled crossover study, and we identified and quantified approximately 60 potential phenolic acid metabolites in urine. Half of the ingested chlorogenic acid and 43% of the tea phenols were metabolized to hippuric acid. Quercetin-3-rutinoside was metabolized mainly to phenylacetic acids, i.e., 3-hydroxyphenylacetic acid (36%), 3-methoxy-4-hydroxyphenylacetic acid (8%) and 3,4-dihydroxyphenylacetic acid (5%). In contrast, in seven humans without a colon, we found only traces of phenolic acid metabolites in urine after they had ingested chlorogenic acid and quercetin-3-rutinoside. This implies that the colonic microflora convert most of these dietary phenols into metabolites that then reach the circulation. Metabolites of dietary phenols have lower antioxidant activity than their parent compounds; therefore, the contribution of dietary phenols to antioxidant activity in vivo might be lower than expected from in vitro tests.

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.

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Effects of the conjugated linoleic acid (CLA) isomers cis-9, trans-11 (c9, t11 CLA) and trans-10, cis-12 (t10, c12 CLA) on lipid metabolism and markers of peroxisome proliferation were investigated in hamsters fed on purified diets containing 30 % energy as fat and 0·1 g cholesterol/kg for 8 weeks. Four groups (n 32 each) received diets without CLA (control), with a mixture of equal amounts of c9, t11 and t10, c12 CLA (CLA mix), with c9, t11 CLA, and with t10, c12 CLA. The total amount of CLA isomers was 1·5 % energy or 6·6 g/kg diet. CLA was incorporated into glycerides and exchanged for linoleic acid in the diet. Compared with the control, the CLA mix and t10, c12 CLA decreased fasting values of LDL- (21 and 18 % respectively) and HDL-cholesterol (8 and 11 %), increased VLDL-triacylglycerol (80 and 61 %), and decreased epididymal fat pad weights (9 and 16 %), whereas c9, t11 CLA had no significant effects. All CLA preparations increased liver weight, but not liver lipids. However, the increase in liver weight was much less in the c9, t11 CLA group (8 %) than in the other two groups (25 %) and might have been caused by the small amount of t10, c12 CLA present in the c9, t11 CLA preparation. Liver histology revealed that increased weight was due to hypertrophy. Markers of peroxisome proliferation, such as cyanide-insensitive palmitoyl CoA oxidase (EC 1.3.3.6) and carnitine acetyl transferase (EC 2.3.1.7) activities, were not increased by CLA. Both c9, t11 CLA and t10, c12 CLA were incorporated into phospholipids and triacylglycerols, but t10, c12 CLA only about half as much as c9, t11 CLA. In addition, linoleic acid and linolenic acid concentrations were lower in lipids of the t10, c12 CLA group compared with the c9, t11 CLA group. These data suggest that t10, c12 CLA stimulated the oxidation of all C18 polyunsaturated fatty acids. The results indicate that the t10, c12 CLA isomer, and not the so-called natural CLA isomer (c9, t11), is the active isomer affecting lipid levels in hamsters.

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