American Journal of Respiratory and Critical Care Medicine

Asthma prevalence has increased dramatically in many countries over recent decades, demonstrating that environmental exposures play a dominant role in the etiology of this disease. Dietary change is one of several causal factors implicated in this trend, and in the past two decades the evidence base on the relation between diet and asthma has increased substantially. In this article we present a perspective on where we believe this literature on asthma is leading, and attempt to identify priorities for further investigation. Our discussion is limited to general effects of diet, and does not address the separate topic of specific food allergy.

Defining and measuring asthma is notoriously difficult, and dietary studies have used many different outcome measures including self-reported diagnosed asthma, symptoms, lung function (particularly FEV1), and airway hyperresponsiveness. In this paper we have concentrated on studies using self-reported diagnosed asthma, wheeze, or airway hyperresponsiveness, because impairment of FEV1 and symptoms of cough and breathlessness, particularly in older individuals, are also strongly associated with chronic obstructive pulmonary disease.

The literature on diet and asthma also covers the full range of levels of evidence, from anecdote and ecological analysis, through cross-sectional and longitudinal observational studies, to randomized controlled clinical trials. As is usually the case, the amount and diversity of evidence decreases with increasing level of study design. Limitations on space in this article preclude a full review of the literature, but thorough and relatively recent reviews are available elsewhere (15) and we will cite these in this article where relevant as sources for reference to the older literature. However, we have also provided assessments of the strength and consistency of the available evidence in tables in this article, fully referenced versions of which are available as an online supplement.

The nutrients most strongly implicated in asthma etiology and their putative mechanisms of action are listed in Table 1

TABLE 1. Nutrients or nutrient groups implicated in the etiology of asthma, and their postulated mechanism of effect


Activity and Potential Mechanisms of Effect
Vitamins A, C, EAntioxidant; protection against endogenous  and exogenous oxidant inflammation
Vitamin CProstaglandin inhibition
Vitamin EMembrane stabilization, inhibition of IgE
Flavones and flavonoidsAntioxidant; mast cell stabilization
MagnesiumSmooth muscle relaxation, mast cell
SeleniumAntioxidant cofactor in glutathione
Copper, zincAntioxidant cofactors in superoxide
n-3 fatty acidsLeukotriene substitution, stabilization
   of inflammatory cell membranes
n-6 polyunsaturated/trans
   fatty acidsIncreased eicosanoid production
Increased smooth muscle contraction
. Although a full discussion of mechanisms is beyond the scope of this review, the dietary factors involved comprise the following main groups (see also Tables 24)

TABLE 2. Amount of evidence, the level of evidence, and consistency of available evidence for the relationship between asthma and fruit or vitamins






Fruit and vegetable intakeLimited evidenceEvidenceLimited evidenceLimited evidenceN/A
No effectMixed resultsMixed resultsMixed results
Vitamin A or beta-caroteneLimited evidenceLimited evidenceEvidenceLimited evidenceLimited evidence
No effectNo effectMixed resultsNo effectMixed results
Vitamin CN/AEvidenceEvidenceLimited evidenceSome evidence
Mixed resultsMixed resultsNo effectNo effect
Vitamin EN/ASome evidenceEvidenceLimited evidenceLimited evidence

No effect
Mixed results
Mixed results

Definition of abbreviations: evidence, > 10 studies; limited evidence, < 5 studies; N/A, no current available evidence; some evidence, 5–10 studies.

For protective, increased risk, or no effect, two-thirds of the studies needed to be in agreement with one another. “Mixed results” was assigned when results where not consistent across the current available research.

TABLE 3. Amount of evidence, the level of evidence, and consistency of available evidence for the relationship between asthma and mineral intakes






SeleniumN/ALimited evidenceEvidenceN/ALimited evidence
No effectProtectiveNo effect
MagnesiumN/ASome evidenceEvidenceN/ALimited evidence
ProtectiveProtectiveNo effect
Copper, zinN/ALimited evidenceEvidenceN/AN/A
Mixed resultsMixed results
SodiumLimited evidenceSome evidenceLimited evidenceN/ASome evidence

Mixed results
No effect
Increased risk

Increased risk

For definition of abbreviations, see Table 2.

For protective, increased risk, or no effect, two-thirds of the studies needed to be in agreement with one another. “Mixed results” was assigned when results where not consistent across the current available research.

TABLE 4. Amount of evidence, the level of evidence, and consistency of available evidence for the relationship between asthma and fatty acids






FishLimited evidenceEvidenceLimited evidenceLimited evidenceN/A
Mixed resultsMixed resultsMixed resultsNo effect
n-3 fatty acidsN/AN/ALimited evidenceLimited evidenceEvidence
Mixed resultsNo effectMixed results
n-6 polyunsaturated/trans fatty acidsLimited evidenceLimited evidenceLimited evidenceLimited evidenceSome evidence

Increased risk
Mixed results
Mixed results
No effect
No effect

For definition of abbreviations, see Table 2.

For protective, increased risk, or no effect, two-thirds of the studies needed to be in agreement with one another. “Mixed results” was assigned when results where not consistent across the current available research.


Vitamin C, vitamin E, and vitamin A/β-carotene are the vitamins most extensively investigated for effects on asthma. All are antioxidants, and vitamins C and E may also have other antiinflammatory or antiallergic effects.

Vitamin C.

Vitamin C is the most extensively investigated and has been shown in several case-control and cross-sectional studies to be associated with a reduced risk of asthma (14, 6, 7), but in the only available substantive longitudinal study, vitamin C intake had no effect on asthma incidence (8). In randomized trials, vitamin C given in combination with other antioxidants protects against ozone-induced bronchoconstriction in asthma (1, 9, 10), but the evidence on the effect of vitamin C given alone is much less conclusive (11, 12). We have recently reported the largest randomized placebo-controlled clinical trial of vitamin C to date, involving 201 patients randomized to vitamin C or placebo for 16 weeks, and found no effect on clinical asthma control (13).

Vitamin E.

Vitamin E effects have been less widely studied and there is relatively little cross-sectional evidence linking vitamin E with asthma (14). There is, however, evidence of an inverse association between vitamin E intake and both allergen skin sensitization and total serum IgE levels in adults (14), and longitudinal evidence that a high vitamin E intake is associated with reduced asthma incidence (8). As cited above, vitamin E is effective when given with other antioxidant vitamins in protecting against ozone effects in asthma (1, 9, 10), but in a recently completed randomized placebo-controlled study of vitamin E supplements for 6 weeks in 72 patients with asthma, we found no evidence of clinical benefit (15).

Vitamin A and β-carotene.

The evidence on vitamin A and/or β-carotene effects is also limited, with some recent cross-sectional studies suggesting a protective effect (14, 6, 16), but no association with asthma incidence in longitudinal study (8). Aside from the ozone studies (1, 9, 10), we are aware of two randomized clinical trials, both from the same research group, reporting evidence of protection against exercise-induced bronchoconstriction after 1 week of supplementation by either a natural source of vitamin A (17), or a food extract rich in the carotenoid lycopene (18).

Several cross-sectional studies have demonstrated a reduced risk of asthma in relation to a high fruit intake (14, 1924), possibly with modification by smoking (25). However, the available longitudinal evidence relates to COPD rather than to asthma (14), and we are not aware of any clinical trials in asthma.

The flavones and flavonoids are naturally occurring antioxidants found particularly in fruits and red wine, which may account for some of the protective effect associated with these foods (14). To date, however, there is only one report suggesting protection by flavones against markers of COPD (26), and no direct epidemiologic or clinical trial evidence relating to asthma.


Selenium is also involved in antioxidant defenses as a coenzyme in glutathione peroxidase. Early case-control studies demonstrated decreased selenium intake and serum levels in patients with asthma in New Zealand (14), and this finding has been confirmed more recently in the United Kingdom (27) but not in Spain (28). We also found no evidence of association between serum selenium levels and airway hyperresponsiveness in adults in the United Kingdom (work published in abstract [29]). The only available randomized placebo-controlled trial involved 14 weeks of supplementation in 24 patients with asthma, and found evidence of improvement in clinical assessments of asthma control in the selenium group but no effect on objective markers of disease (30).


Magnesium has several biological effects of potential relevance to asthma, including bronchodilatation when given intravenously in acute severe asthma (31). There is also strong cross-sectional epidemiologic evidence of protection by dietary magnesium against asthma (14), but our recent randomized placebo-controlled trial of magnesium supplementation showed no evidence of benefit after 4 months of supplementation (13). At least one other substantive clinical trial, to our knowledge published only in abstract, is also negative (32).


Early epidemiologic evidence suggesting that a high sodium intake may be associated with increased airway responsiveness (14) has led to several intervention studies of sodium supplementation and/or restriction. The research suggests that the effects of sodium are limited to individuals with asthma; however, current research has not provided conclusive evidence that sodium restriction improves asthma (33, 34), though at least one study suggests that sodium loading exacerbates hyperresponsiveness (35).

Copper, zinc, and other minerals.

There is limited evidence linking copper, zinc, and other elements (such as manganese) with asthma (14), but we are not aware of any relevant clinical trials. The role of these nutrients thus remains unclear.

Research into fatty acid effects has focused on two main areas: intake of omega-3 polyunsaturated fatty acids from fish oils, which is potentially beneficial, and of omega-6 and trans-fatty acids, which may be detrimental to asthma (14). The observational evidence on fish oil effects has been relatively consistent in demonstrating protection against asthma and/or allergy in relation to a high intake (14), though the clinical trial evidence is less strongly conclusive (36, 37). Similarly, ecological and other cross-sectional data support the hypothesis that omega-6 acids may increase asthma risk (3840), and other studies indicate that full fat cream and butter (rich in saturated fats) is associated with a reduced risk of asthma in young children (21, 41). However, there are no relevant intervention studies.

In this article we have passed over the considerable literature, predominantly cross-sectional, linking reduced lung function to a low intake of antioxidant vitamins, fruits, flavones, and magnesium (14). There are also longitudinal studies providing evidence that a high intake of fruits and vitamin C is associated with a reduced rate of decline in FEV1 over time (4244), though with no evidence of an effect of magnesium intake (44). These studies thus provide support for the hypothesis that fruits and/or their constituents may protect against COPD, but are not specific to asthma.

There have been three major nutrient intervention trials in which the supplement has consisted of multinutrients, all of which were designed to address other primary hypotheses, but have also provide data on relevant respiratory outcomes. The Alpha-Tocopherol Beta-Carotene Cancer Prevention Study randomized over 29,000 adults to receive either d1-α-tocopherol, β-carotene, both, or placebo for 5 to 8 years and found that supplementation did not decrease the incidence or recurrence of symptoms of cough, sputum production, or dyspnea (45). In the Carotene and Retinol Efficacy Trial, there was no difference in rate of lung function decline over 11 years in over 18,000 subjects randomized to β-carotene and retinyl palmitate, or placebo (study reported, to our knowledge, only in abstract [46]). Most definitive is the Heart Protection Study, a trial of the effect of 5 years' supplementation with antioxidant vitamins (vitamin E, vitamin C, and β-carotene, or a matching placebo) on major coronary events in over 20,000 adults (47). FEV1 and FVC, and hospitalizations for asthma or COPD during the 5-year study period, were assessed as secondary outcomes at the end of the study, and no differences were found (47). These three intervention trials are thus conclusive in demonstrating no appreciable effect of antioxidant vitamin supplements on markers of COPD and/or asthma, and therefore question the likelihood that further supplementation studies with these nutrients are likely to demonstrate any benefit.

Although far from complete in relation to all of the above nutrients, there is a consistent theme in the evidence cited above, which is that although a wide range of nutrients appear to have an effect on asthma outcomes in cross-sectional study, evidence from longitudinal studies and randomized clinical trials is far less consistent or conclusive. Indeed, in longitudinal study only vitamin E has been shown to have a protective effect on asthma (8), whereas in clinical trials no effect has been demonstrated for vitamin E on asthma control (15, 47). The clinical trial evidence on vitamin C and magnesium also implies no effect on asthma (13), and for other nutrients is based on small numbers and/or relatively weak outcomes (17, 18, 30). Although shown to protect the airway against ozone effects therefore (1, 9, 10), it appears that the hypothesis that individual nutrients alone or in combination have a major impact on clinical asthma severity or incidence is far from proved. It is therefore important to consider the possible explanations for the inconsistencies in the evidence, and there are several.

Lack of Available Evidence

For many of the diet–asthma associations, understanding is limited by a current lack of evidence. This is particularly true for determining the longitudinal effect of diet on asthma, especially as diet may potentially have different roles in the incidence of asthma and severity of disease.

False Positives Arising from Multiple Hypothesis Testing

Much of the cross-sectional work on diet and asthma has been performed by secondary analysis of existing datasets. Particularly in older publications, it is often unclear whether the dietary associations reported arose as a result of testing a genuine a priori hypothesis, or from a hypothesis-generating analysis of the available data. It is likely that many of the single nutrient associations with disease reported to date are indeed false positives arising from multiple hypothesis testing by different, if not the same, investigators.

Measurement Issues

Diet is complex and measurement is difficult. Food-frequency questionnaires, 24-house diet recall, examination of individual food items, food patterns, serum nutrients, and other methods all have their relative strengths and weaknesses, all can introduce substantial misclassification, and the close correlation of many nutrients presents problems when trying to identify independent nutrient effects. Part of the difficulty of interpreting dietary studies is likely to arise from measurement errors and biases inherent in the methods used.


The potential for confounding in cross-sectional and longitudinal studies of diet and asthma is substantial, particularly because the sources of many of the above nutrients are the perceived “healthy” foods—such as fruits and green vegetables—are also relatively rich in other antioxidant vitamins, flavones and flavonoids, magnesium, and other potentially beneficial nutrients. To deal with this, it is necessary to control for other nutrient effects in analysis, but because of the strong correlation between nutrient intakes this demands sample sizes that are typically far in excess of most of those reported to date. Few if any of the available studies has attempted to control for the full range of nutrients potentially involved, and in our view none has succeeded. Diet is also strongly related to other recognized determinants of asthma risk, such as smoking and socioeconomic status, and depending on the quality of the available measures, controlling for these confounders can also be difficult. Confounding is therefore likely to be a major problem in much of the observational work.

Single Nutrient Supplements May Be Ineffective

It is also possible that any beneficial effect of diet is mediated through the combined effect of several nutrients, rather than any one or small group alone. The implication of this is that any further studies of nutrient supplementation should pursue an extensive “polypill” approach, delivering a cocktail of potentially beneficial nutrients, rather than the single or limited combinations tested to date. The ozone studies (1, 9, 10) provide some evidence that this may indeed be the case, though the lack of any impact of an antioxidant vitamin cocktail on asthma admissions in the Heart Protection Study suggests that the protective effect on acute airway responses does not translate into clinical benefit (47).

Supplements May Also Be Harmful

It is also possible that dietary antioxidants also have prooxidant activity (48). If so, any net benefit of supplementation might be restricted to patients and populations that are relatively depleted in antioxidants, whereas in less depleted individuals this benefit may be counterbalanced by prooxidant actions. To date there is no strong evidence that this is the case in relation to asthma.

Other Nutrient Effects May Be More Important

Another implication of the confounding argument above is that if diet has an effect on asthma, the nutrients responsible may not those that have been widely studied to date. Increased understanding of the role of different nutrients in maintaining antioxidant defense, such as the phenolic lipids, may open up new areas of nutrient research that prove more productive.

It Is Foods Rather than Individual Nutrients that Matter

The benefit of diet for asthma may be from combined nutritional value in particular foods of the combined interaction of foods or combined effect of foods in a healthy diet. The clear and obvious extension to the above is that the best way to deliver a suitably comprehensive and synergistic range of nutrients is to supplement the diet with foods that provide the best combination of nutrients, such as fresh fruits and vegetables. We are currently assessing the effect of fruit supplementation on the prevalence of asthma in young children, capitalizing on a natural experiment arising from the phased introduction by the UK government of a scheme providing all 4- to 6-year-old children with a free portion of fruit every day at schools. Data comparing asthma incidence and prevalence between children who commenced the scheme in 2004 and those who did not will be available during 2005. We are not aware of any other fruit supplementation trials with respiratory outcomes in progress.

Genetic Susceptibility May Be Important

It is also likely that genetic factors, as for example polymorphisms in the glutathione S-transferase gene (49), determine susceptibility to oxidant damage and to benefit from antioxidant supplementation. Further work is necessary to elucidate this and other potential genetic influences.

Diet Acts through Programming Disease Risk in Early Life

It is possible that the effects of diet on lung disease outcomes arise from effects occurring in prenatal or very early life, and are apparent in cross-sectional studies later in life because broad dietary habits tend to track through life. If so, dietary effects would be expected to be evident in cross-sectional and longitudinal studies, but not in intervention trials in adults, as the period of intervention would need to be in early life. There is to date relatively little evidence regarding dietary intervention during pregnancy and/or infancy, though some recent clinical trials indicate promise with omega-3 fatty acid supplementation (5, 50, 51).


Our interpretation of the evidence and the above arguments is that if diet plays an important role in asthma, the most likely and most efficient method of exploiting that effect to individual and population benefit is probably dietary manipulation to increase intake of natural foods, and particularly fresh fruits and vegetables, in a balanced diet throughout life. This is not only the most logical and pragmatic interpretation, it is also the strategy most likely to yield benefits in other disease areas. The way forward, we believe, is therefore in dietary manipulation rather than a continued search for, and attempts to intervene in, individual nutrient effects. However, general advice on diet for patients with asthma needs to be based on evidence rather than supposition, and it is therefore important that the effects of dietary change on lung health are properly tested in appropriate trial designs.

1. Fogarty A, Britton J. The role of diet in the aetiology of asthma. Clin Exp Allergy 2000;30:615–627.
2. Smit HA, Grievink L, Tabak C. Dietary influences on chronic obstructive lung disease and asthma: a review of the epidemiological evidence. Proc Nutr Soc 1999;58:309–319.
3. Romieu I, Trenga C. Diet and obstructive lung diseases. Epidemiol Rev 2001;23:268–287.
4. Smit HA. Chronic obstructive pulmonary disease, asthma and protective effects of food intake: from hypothesis to evidence. Respir Res 2001;2:261–264.
5. Spector SL, Surette ME. Diet and asthma: has the role of dietary lipids been overlooked in the management of asthma? Ann Allergy Asthma Immunol 2003;90:371–377.
6. Harik-Khan RI, Muller DC, Wise RA. Serum vitamin levels and the risk of asthma in children. Am J Epidemiol 2004;159:351–357.
7. Rubin RN, Navon L, Cassano PA. Relationship of serum antioxidants to asthma prevalence in youth. Am J Respir Crit Care Med 2004;169:393–398.
8. Troisi RJ, Willett WC, Weiss ST, Trichopoulos D, Rosner B, Speizer FE. A prospective study of diet and adult-onset asthma. Am J Respir Crit Care Med 1995;151:1401–1408.
9. Romieu I, Sienra-Monge JJ, Ramirez-Aguilar M, Tellez-Rojo MM, Moreno-Macias H, Reyes-Ruiz NI, Rio-Navarro BE, Ruiz-Navarro MX, Hatch G, Slade R, et al. Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants. Am J Respir Crit Care Med 2002;166:703–709.
10. Trenga CA, Koenig JQ, Williams PV. Dietary antioxidants and ozone-induced bronchial hyperresponsiveness in adults with asthma. Arch Environ Health 2001;56:242–249.
11. Hatch GE. Vitamin C and asthma. In: Vitamin C in health and disease. Packer L, Fuchs J, editors. 1997. New York: Marcel Dekker, p. 279–294.
12. Ram FSF, Rowe BH, Kaur B. Vitamin C supplementation for asthma (Cochrane Review). In: The Cochrane Library, Issue 1. 2004. Chichester, UK: John Wiley & Sons, Ltd.
13. Fogarty A, Lewis SA, Scrivener SL, Antoniak M, Pacey S, Pringle M, Britton J. Oral magnesium and vitamin C supplements in asthma: a parallel group randomized placebo-controlled trial. Clin Exp Allergy 2003;33:1355–1359.
14. Fogarty A, Lewis S, Weiss S, Britton J. Dietary vitamin E, IgE concentrations, and atopy. Lancet 2000;356:1573–1574.
15. Pearson PJK, Lewis SA, Britton J, Fogarty A. Vitamin E supplements in asthma: a parallel group randomised placebo-controlled trial. Thorax (In press)
16. Huang SL, Pan WH. Dietary fats and asthma in teenagers: analyses of the first Nutrition and Health Survey in Taiwan (NAHSIT). Clin Exp Allergy 2001;31:1875–1880.
17. Neuman I, Nahum H, Ben Amotz A. Prevention of exercise-induced asthma by a natural isomer mixture of beta-carotene. Ann Allergy Asthma Immunol 1999;82:549–553.
18. Neuman I, Nahum H, Ben Amotz A. Reduction of exercise-induced asthma oxidative stress by lycopene, a natural antioxidant. Allergy 2000;55:1184–1189.
19. Antova T, Pattenden S, Nikiforov B, Leonardi GS, Boeva B, Fletcher T, Rudnai P, Slachtova H, Tabak C, Zlotkowska R, et al. Nutrition and respiratory health in children in six Central and Eastern European countries. Thorax 2003;58:231–236.
20. Gilliland FD, Berhane KT, Li YF, Gauderman WJ, McConnell R, Peters J. Children's lung function and antioxidant vitamin, fruit, juice, and vegetable intake. Am J Epidemiol 2003;158:576–584.
21. Woods RK, Walters EH, Raven JM, Wolfe R, Ireland PD, Thien FC, Abramson MJ. Food and nutrient intakes and asthma risk in young adults. Am J Clin Nutr 2003;78:414–421.
22. Priftanji AV, Qirko E, Burr ML, Layzell JCM, Williams KL. Factors associated with asthma in Albania. Allergy 2002;57:123–128.
23. Heinrich J, Holscher B, Bolte G, Winkler G. Allergic sensitization and diet: ecological analysis in selected European cities. Eur Resp J 2001;17:395–402.
24. Forastiere F, Pistelli R, Sestini P, Fortes C, Renzoni E, Rusconi F, Dellorco V, Ciccone G, Bisanti L. Consumption of fresh fruit rich in vitamin C and wheezing symptoms in children. Thorax 2000;55:283–288.
25. Butland BK, Strachan DP, Anderson HR. Fresh fruit intake and asthma symptoms in young British adults: confounding or effect modification by smoking? Eur Resp J 1999;13:744–750.
26. Tabak C, Arts IC, Smit HA, Heederik D, Kromhout D. Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones: the MORGEN Study. Am J Respir Crit Care Med 2001;164:61–64.
27. Shaheen SO, Sterne JA, Thompson RL, Songhurst CE, Margetts BM, Burney PG. Dietary antioxidants and asthma in adults: population-based case- control study. Am J Respir Crit Care Med 2001;164:1823–1828.
28. Picado C, Deulofeu R, Lleonart R, Agusti M, Mullol J, Qunito L, Torra M. Dietary micronutrients/antioxidants and their relationship with bronchial asthma severity. Allergy 2001;56:43–49.
29. Britton J, Pavord I, Richards K, Knox A, Wisniewski A, Weiss S, Tattersfield A. Blood selenium, copper, vitamins C and E and airway hyperreactivity [abstract]. Am J Respir Crit Care Med 1995;151:A470.
30. Hasselmark L, Malmgren R, Zetterstrom O, Unge G. Selenium supplementation in intrinsic asthma. Allergy 1993;48:30–36.
31. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CAJ. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department (Cochrane Review). In: The Cochrane Library, Issue 1. 2004. Chichester, UK: John Wiley & Sons, Ltd.
32. Grebski E, Hacki M, Hinz G, Medici TC. The effects of magnesium supplementation on lung function and eosinophilic inflammation in asthma [abstract]. Am J Respir Crit Care Med 2000;161:A607.
33. Ram FSF, Ardern KD. Dietary salt reduction or exclusion for allergic asthma (Cochrane Review). In: The Cochrane Library, Issue 1. 2004. Chichester, UK: John Wiley & Sons, Ltd.
34. Mickleborough TD, Gotshall RW, Cordain L, Lindley M. Dietary salt alters pulmonary function during exercise in exercise-induced asthmatics. J Sports Sci 2001;19:865–873.
35. Carey OJ, Locke C, Cookson JB. Effect of alterations of dietary sodium on the severity of asthma in men. Thorax 1993;48:714–718.
36. De Luca S, Woods R, Thien FCK, Abramson MJ. Dietary marine fatty acids (fish oil) for asthma in adults and children (Cochrane Review). In: The Cochrane Library, Issue 1. 2004. Chichester, UK: John Wiley & Sons, Ltd.
37. Mickleborough TD, Murray RL, Ionescu AA, Lindley MR. Fish oil supplementation reduces severity of exercise-induced bronchoconstriction in elite athletes. Am J Respir Crit Care Med 2003;168:1181–1189.
38. Bolte G, Frye C, Hoelscher B, Meyer I, Wjst M, Heinrich J. Margarine consumption and allergy in children. Am J Respir Crit Care Med 2001;163:277–279.
39. Dunder T, Kuikka L, Turtinen J, Rasanen L, Uhari M. Diet, serum fatty acids, and atopic diseases in childhood. Allergy 2001;56:425–428.
40. Heinrich J, Holscher B, Bolte G, Winkler G. Allergic sensitization and diet: ecological analysis in selected European cities. Eur Resp J 2001;17:395–402.
41. Wijga AH, Smit HA, Kerkhof M, de Jongste JC, Gerritsen J, Neijens HJ, Boshuizen HC, Brunekreef B. Association of consumption of products containing milk fat with reduced asthma risk in pre-school children: the PIAMA birth cohort study. Thorax 2003;58:567–572.
42. Butland BK, Fehily AM, Elwood PC. Diet, lung function, and lung function decline in a cohort of 2512 middle aged men. Thorax 2000;55:102–108.
43. Carey IM, Strachan D, Cook DG. Effects of changes in fresh fruit consumption on ventilatory function in healthy British adults. Am J Respir Crit Care Med 1998;158:728–733.
44. McKeever TM, Scrivener S, Broadfield E, Jones Z, Britton J, Lewis SA. Prospective study of diet and decline in lung function in a general population. Am J Respir Crit Care Med 2002;165:1299–1303.
45. Rautalahti M, Virtamo J, Haukka J, Heinonen OP, Sundvall J, Albanes D, Huttunen JK. The effect of Alpha-Tocopherol and Beta-Carotene supplementation on COPD symptoms. Am J Respir Crit Care Med 1997;156:1447–1452.
46. Balmes J, Ngo L, Keogh J, Cullen M, Brodkin C, Williams J, Reddich C, Omenn G, Barnhart S. Effect of supplemental B-carotene and retinol on rate of decline in lung function. Am J Respir Crit Care Med 1998;157:A46. (Abstract).
47. Collins R, Armitage J, Parish S, Sleight P, Peto R. MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002;360:23–33.
48. Podmore ID, Griffiths HR, Herbert KE, Mistry N, Mistry P, Lunec J. Vitamin C exhibits pro-oxidant properties. Nature 1998;392:559.
49. Fryer AA, Bianco A, Hepple M, Jones PW, Strange RC, Spiteri MA. Polymorphism at the glutathione S-transferase GSTP1 locus: a new marker for bronchial hyperresponsiveness and asthma. Am J Respir Crit Care Med 2000;161:1437–1442.
50. Dunstan JA, Mori TA, Barden A, Beilin LJ, Taylor AL, Holt PG, Prescott SL. Maternal fish oil supplementation in pregnancy reduces interleukin-13 levels in cord blood of infants at high risk of atopy. Clin Experiment Allergy 2003;33:442–448.
51. Mihrshahi S, Peat JK, Marks GB, Mellis CM, Tovey ER, Webb K, Britton WJ, Leeder SR. Eighteen-month outcomes of house dust mite avoidance and dietary fatty acid modification in the Childhood Asthma Prevention Study (CAPS). J Allergy Clin Immunol 2003;111:162–168.
Correspondence and requests for reprints should be addressed to John Britton, M.D., University of Nottingham, Division of Epidemiology and Public Health, City Hospital, Nottingham, NG5 1PB UK. E-mail:


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