In this large prospective cohort of US men, two distinct dietary patterns were identified using principal component analysis: the prudent pattern (loaded by a high consumption of fruits, vegetables, fish and whole grains) and the Western pattern (loaded by a high intake of refined grains, cured and red meats, desserts and sweets and French fries). During 12 years of follow‐up, the risk of newly diagnosed COPD decreased as the prudent pattern score increased, whereas the risk of newly diagnosed COPD increased as the Western pattern score increased.
Studies on the association of individual foods and nutrients and COPD have suggested a beneficial effect of antioxidants—particularly vitamin C and, to a lesser extent, vitamin E—on COPD or FEV1
However, there is no clear association between one particular food and COPD. Data from the β‐Carotene and Retinol Efficacy Trial (CARET) conducted in the US which included 18
341 heavy smokers and asbestos workers also indicated that vitamin A supplementation had no effect on the rate of decline of lung function in smokers and former smokers.22
Data from the α‐tocopherol and β‐carotene Cancer Prevention Study (ATBC Study) conducted in Finland on 29
133 men aged 50–69 years who were heavy smokers showed no reduction in COPD symptoms in those receiving β‐carotene or α‐tocopherol supplements.23
Preliminary results from the Feasibility of Retinoids in the Treatment of Emphysema (FORTE) study, a multicentre clinical trial conducted in the US which included about 150 patients with emphysema, showed no change in respiratory symptoms, lung function testing, and CT scan lung density after supplementation with retinoic acid.24
Although the effect of any individual nutrient in reducing the risk of COPD may be too small to detect, as suggested by these negative results, when several nutrients are consumed together, the cumulative effect may be sufficient for detection. Indeed, considering diet by an overall approach rather than by specific foods or nutrients may suggest a more comprehensive approach to disease prevention.
In this context, dietary patterns provide an overview of diet and are a good way to assess the relation between diet and newly diagnosed COPD. Dietary patterns have been investigated in relation to several diseases such as cardiovascular diseases,19
but few studies have examined the relationship between dietary patterns and respiratory diseases. Butler et al
identified two patterns in 52
325 adult Chinese Singaporean men and women aged 45–74 years: one “vegetable, fruit, soy” pattern and one “meat‐dim sum” pattern, corresponding to a high intake of chicken, pork, fish, rice and noodle dishes, and preserved foods.18
The “meat‐dim sum” pattern was associated with an increased risk of incident cough with phlegm. The second study was performed by our group in the Nurses' Health Study (unpublished data). Briefly, we identified two dietary patterns among 71
871 women aged 30–55 years in 1976: a prudent pattern highly loaded by intake of fruits, vegetables, fish and whole grain products, and a Western pattern highly loaded by intake of refined grains, processed and red meats, desserts and French fries. We found that the prudent pattern was associated with a decreased risk of newly diagnosed COPD between 1984 and 2000 and, by contrast, that the Western pattern was associated with an increased risk of newly diagnosed COPD.
Although the diet and lifestyle of Chinese Singaporeans are different from those in the US population, these findings are consistent with those from the female nurses and from the current study of male health professionals. All three studies suggest a deleterious effect of a diet rich in meat, starchy foods and high‐fat dairy products on COPD. The Western diet is highly loaded by processed meats, one of the most important compounds of which is nitrite. Nitrites generate reactive nitrogen species which provoke nitrosative stress; this may contribute to the progressive deterioration in pulmonary function.25
The Western diet also was loaded by a high intake of foods with a high glycaemic index (refined grains, desserts, sweets). It has been suggested that hyperglycaemia is related to impaired lung function,26
which remains the main measurement for diagnosis of COPD.27
Furthermore, both hyperglycaemia and COPD are positively related to inflammation,28,29
even if the causal association between COPD and systemic inflammation remains unclear.30
As several foods from the Western diet (such as cured meat and refined grains) might be related to COPD, the Western pattern offers a good way of summarising the possible effects of these diverse but highly correlated foods.
The finding that the prudent pattern (loaded by fruits and vegetables) is associated with a decreased risk of newly diagnosed COPD is consistent with previous epidemiological literature suggesting a beneficial effect of antioxidants—particularly vitamin C and, to a lesser extent, vitamin E—on COPD or FEV1
Butler et al18
also reported a weak association between their fruits‐vegetables‐soy pattern and cough with phlegm which disappeared after adjustment for non‐starch polysaccharide. Non‐starch polysaccharide is a major component of dietary fibre and of some non‐citrus fruits. In our study, whole grain products are included in the prudent pattern. Although the consumption of fibre and whole grain has not been studied to any extent in relation to COPD, Butler et al
reported in this population of Singaporean Chinese that a diet high in fibre may reduce the incidence of cough with phlegm.31
In a cross‐sectional study, Tabak et al32
reported a positive association between whole grain consumption and the prevalence of COPD in 13
651 men from the MORGEN study. The prudent pattern also was loaded by a high intake of fish, one of the main sources of omega‐3 polyunsaturated fatty acids, but the results are still inconsistent across studies5
and the only published prospective study observed no relation between intake of omega‐3 and the incidence of chronic non‐specific lung disease.9
Principal component analysis to derive dietary patterns involves several arbitrary decisions on the selection of included variables, the construction of the food groups, the number of retained factors, the method of rotation and the labels of the factors.33
In this cohort of men, multiple sensitivity analyses were performed to assess the reproducibility and the robustness of these dietary patterns.17
Similar patterns were identified after using the maximum likelihood method instead of the principal component method to extract initial factors, after using an oblique rotation instead of an orthogonal one, after retaining three patterns instead of two, and even after deriving dietary patterns based on the 131 individual food items rather than from the predefined food groups.17
In addition to these statistical considerations, our study has other potential limitations. First, we acknowledge that the association between dietary patterns and newly diagnosed COPD may be due in part to a residual confounding by cigarette smoking. To minimise this possibility, multivariate models were adjusted with multiple measures of tobacco exposure (smoking habits, pack‐years and (pack‐years)2
), but residual confounding by smoking remains a possibility. Furthermore, we were not able to adjust for environmental tobacco smoke, which remains an important risk factor for COPD.34
However, analyses were adjusted for environmental tobacco smoke in the Nurses' Health Study and it did not change the result (unpublished data). Second, newly diagnosed COPD was defined by a self‐reported physician diagnosis of COPD and no lung function results were available. However, the questionnaire‐based definition of newly diagnosed COPD was validated in a subset of a similar population of female health professionals.21
The low rate of COPD in this population is probably due to the low smoking rates among health professionals. The main source of misclassification was a misdiagnosis with asthma, but our findings for asthma diagnosis were null. While we acknowledge the potential for some misclassifications, these data allowed us to investigate the relationship between dietary patterns and COPD in a very large population, with repeated measurements of both diet and COPD. Finally, due to the relatively small number of cases (n
111), it was not possible to perform stratified analyses according to smoking status or BMI. BMI is considered as a marker of low‐grade systemic inflammation, and we would have liked to examine possible effect modification by this factor. Celli et al
have recently suggested that BMI is an important factor in the severity of COPD,35
and in the Nurses' Health Study we reported a significant interaction between BMI and the Western pattern. The association between the Western pattern and the risk of newly diagnosed COPD was stronger in lean women (BMI
) than in others, but the mechanism for the observed interaction requires further study.
In summary, we report the first study on dietary patterns in relation to the risk of newly diagnosed COPD in men. We identified two major dietary patterns—the prudent and the Western patterns—and found that both were associated with a risk of newly diagnosed COPD. The prudent pattern was negatively associated with the risk of newly diagnosed COPD while the Western pattern was positively associated with the risk of newly diagnosed COPD. Temporal changes in dietary patterns may contribute to ongoing increases in COPD.