The objectives of the present study were to determine the feasibility of using manufactured foods, enriched with eicosapentaenoic acid (EPA) and docosahexaenoic acid(DHA) as a means of increasing the intake of these n−3 polyunsaturated fatty acids (PUFA), and to determine the effect of the consumption of these foods on postprandial lipaemia and other metabolic responses to a high-fat mixed test meal. Nine healthy, normotriacylglycerolaemic, free-living male volunteers (aged 35–60 years) completed the randomized, controlled, single-blind, crossover study. The study consisted of two periods (each of 22d) of dietary intervention, separated by a 5-month washout period. During these two periods the subjects were provided with the manufactured foods enriched with EPA and DHA (n−3 enriched) or identical but unenriched foods (control). A mixed test meal containing 82g fat was given to the fasted subjects on day 22 of each dietary intervention period. Two fasting, and thereafter hourly, blood samples were collected from the subjects for an 8h period postprandially. Plasma triacylglycerol, total and HDL-cholesterol, non-esterified fatty acids (NEFA), glucose and immunoreactive insulin levels, post-heparin lipoprotein lipase (EC 188.8.131.52) activity and the plasma free fatty acid and phospholipid fatty acid compositions were measured. A mean daily intake of 1·4 g EPA + DHA (0·9 g EPA, 0·5 g DHA) was ingested during the n−3-enriched dietary period, which was significantly higher than the intake during the habitual and control periods (P <0·001) assessed by a 3 dweighed food intake. A significantly higher level of EPA + DHA enrichment of the plasma fatty acids and phospholipids (P < 0·001) after the n−3-enriched compared withthe control intervention periods was also found. The energy intake on both of the dietary intervention periods was found to be significantly higher than on the habitual diet (P <0·001), with an increase in body weight of the subjects, which reachedsignificance during the n−3 PUFA-enriched dietary intervention period (P < 0·04). The palatability of the enriched foods was not significantly different from that of the control foods. Significantly higher fasting plasma HDL-cholesterol and glucose concentrations were found after the n-3 PUFA-enriched compared with the control intervention period (P < 0·02 and P < 0·05 respectively). No significant differences were found for the postprandial lipid and hormone measurements, except for significantly lower levels of NEFA at 60min after the n−3-enriched intervention period (P< 0·04). Enriched manufactured foods were a feasible vehicle for increasing n−3 PUFA intake. However the nature of the foods provided as the n−3 vehicle may have contributed to the increased body weight and higher energy intakes which were adverse consequences of the intervention. These factors, together with the short duration of the study may have been reponsible for the failure to observe significant plasma triacylglycerol reductions in response to daily intakes of 1·4g EPA+DHA.