The epidemiological evidence for a relationship between diet and indicators of asthma and chronic obstructive pulmonary disease (COPD) is evaluated. The review focuses on the intake of Na, n−3 fatty acids, and antioxidant vitamins as well as fruit and vegetables. Experimental studies suggest that a high-Na diet has a small adverse effect on airway reactivity in asthma patients. However, observational studies provide no clear evidence that high Na intake has adverse effects on airway reactivity or asthma symptoms in open populations. n−3 Polyunsaturated fatty acids, which are present in fish oils, are metabolized into less broncho-constricting and inflammatory mediators than n−6 polyunsaturated fatty acids. Studies in the general adult population suggest that a high fish intake has a beneficial effect on lung function, but the relationship with respiratory symptoms and clinically-manifest asthma or COPD is less evident. Also, experimental studies in asthma patients have not demonstrated an improvement in asthma severity after supplementation with fish oil. Several studies showed a beneficial association between fruit and vegetable intake and lung function, but the relationship with respiratory symptoms and the clinically-manifest disease was less convincing. A similar pattern was found for vitamin C in relation to indicators of asthma and COPD, but there are still conflicting results with respect to vitamin E and β-carotene. In conclusion, the epidemiological evidence for a beneficial effect on indicators of asthma and COPD of eating fish, fruit and vegetables is increasing. However, the effectiveness of dietary supplementation in open-population samples is often not demonstrated. Several unresolved questions are raised, which should be addressed in future studies on the relationship between diet and respiratory disease.

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 3.1.1.34) 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.