Alternate Healthy Eating Index 2010 and risk of chronic obstructive pulmonary disease among US women and men: prospective studyBMJ 2015; 350 doi: https://doi.org/10.1136/bmj.h286 (Published 03 February 2015) Cite this as: BMJ 2015;350:h286
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We thank Young et al. for their interest in our recently published paper.
Regarding the first question raised by the authors about the magnitude of the association between AHEI-2010 score on risk of COPD, as compared with cohort studies of other chronic diseases, we reported a 33% lower risk for those higher (versus lower) AHEI-2010 scores. This is little bit stronger perhaps but generally consistent with previous studies looking at the association between AHEI-2010 and risk of developing chronic diseases (19%) , obesity (24%) , type 2 diabetes (13%) , epithelial ovarian cancer (15%) , and all-cause mortality (24%) . The observed 33% reduction is of similar magnitude to the favorable association of higher AHEI-2010 score with healthy ageing and well-being (34%) .
Regarding the second question, even if we decided to investigate the individual role of each component score of the AHEI-2010, we believe that a healthy diet based on the overall AHEI-2010 is recommended to improve lung health, because all these individual items are strongly correlated. When we investigated the individual role of each component, we adjusted for the 10 others items to account for these correlations.
Regarding the third and final question raised by Young et al., we reported a non-significant negative association between whole grain intake and the risk of COPD (RR 0.82, 95%CI 0.48 to 1.38). We are less concerned about confounding by cured meat intake or smoking exposure. As stated in our publication, we faced a statistical power issue in the men (e.g., there were only 24 cases in the fifth quintile of whole grains intake). We hope that additional research on this topic will help to clarify these important issues.
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Competing interests: No competing interests
In their recent paper, Varraso and colleagues show in two large prospective studies of men and women, a healthy diet confers a protective effect on the development of COPD (HR=0.67 for highest vs lowest/least healthy diet quintile).1 This finding persisted after adjustment for smoking (HR=0.69 and HR=0.50 for current and former smokers respectively) and was present in both genders (HR=0.69 and HR=0.60 for women and men respectively). Although slightly greater in magnitude in men compared to women, the protective effect failed to achieve significance due under-powering from 4 fold fewer COPD cases in men (167 vs 723). This gender effect persisted after stratification by smoking status, where the magnitude of the protective effect was even greater in ex-smokers compared to current smokers (HR=0.52 for women and HR=0.0.44 for men, and HR=0.70 for women and HR=0.64 for men, respectively). These findings raise 3 important questions outlined below.
Given all that has been written about healthy diets and reduced risk of coronary heart disease and cancers, it is refreshing to see comparable studies now focussing on lung health, and in particular susceptibility to COPD.1,2 We have previously suggested that a reduced FEV1, the characteristic marker of COPD, is likely a barometer of a generalised susceptibility to heavy oxidant exposure (particularly from smoking in the case of COPD) and/or disposition to pulmonary-systemic inflammation (in part driven by genetic susceptibility).3 As the lung is a very vascular organ, with a closely apposed air-capillary interface, it is perhaps of no surprise that a healthy diet also confers protection for COPD, where both pro-oxidant and pro-inflammatory pathogenic mechanisms have been strongly implicated. The first question is “How does the magnitude of the protective effect on COPD (HR=0.67 or 33% reduction) compare with other prospective studies of other chronic diseases using the same dietary tool?” We note reductions in all-cause mortality, cardiovascular mortality and cancer mortality for men and woman (HR=0.76 both genders, HR=0.71 and 0.72 for men and women respectively, and HR=0.82 and 0.88 for men and women respectively).4
In a detailed breakdown of their dietary assessment tool, Varraso and colleagues identify differences in whole grain intake as the single most important driver of the protective effect of diet on susceptibility to COPD. In contrast, fruit and vegetables did not show a comparable protective effects as previously described,5 although they did find that fruit conferred a 20% reduction (with a trend to significance). The second question is “How closely correlated are these component scores (fruit, vegetables, whole grain and red meat) to each other and what happens to the overall healthy diet effect (HR=0.67) when a high whole grain intake is “adjusted” or controlled for in the analysis?” Whole grains are notable for their high fibre content which has been associated with lower risk of COPD in several other prospective studies.6,7 We have previously suggested that high fibre diets may confer their protective effect on COPD through alteration of colonic bacteria, increased synthesis of of naturally occurring anti-inflammatory compounds (small chain fatty acids) absorbed in to the portal circulation and inhibition of HMGCoA reductase and/or histone deacetylase in the liver.7 If this were true, it would put systemic inflammation and the Gut-Liver-Lung axis front and center of COPD pathophysiology.8 It would also suggest that primary or secondary prevention of COPD through inhibition of pulmonary-systemic inflammation makes good sense, and that this is achievable through diet or pharmacological interventions (such as with statins).9,10
After stratification by gender, the protective effect of whole grains on COPD is stronger in women than men (HR=0.67 and HR=0.82 respectively), with again no apparent gender effect for fruit or vegetable intakes. Women generally smoke less intensely than men (cigs/day), although rates of “current smoker” in nurses are 2 fold higher than doctors.11 This leads us to propose the protective effect of whole grain in women may be greater because they continue to smoke into their midlife. The only other significant protective effect on COPD, after stratification by gender, was from low intake of red/processed meat in men (HR=0.47), not evident in women (HR=0.88). This processed meat effect has also been reported by others with regards to risk of COPD and could possibly interact inversely with whole grain intake.12 The last question is “Has the protective effect of whole grains in men been “offset” by their higher intake of red/processed meat and/or more intense smoking exposure?”
We appreciate that due to the small number of COPD cases in this study, the HR estimates have overlapping confidence intervals after stratification by gender and smoking status. We also appreciate that the relationships between the overall dietary scores and scores from individual components is likely to be complex. However, the results of the study from Varraso and colleagues suggests to us that dietary fibre is the most important dietary constituent to confer a protective effect on COPD and that this effect maybe modified by smoking and possibly red meat consumption. The public health implications of this study are considerable and we are hopeful that the investigators can answer these questions and, in doing so, provide greater clarity around the dietary benefits of fibre on susceptibility to COPD.
1. Varraso R, Chiuve SE, Fung TT, et al. Alternate Healthy Eating Index 2010 and risk of chronic obstructive pulmonary disease among US women and men: prospective study. BMJ 2015; 350:h286/ doi:10.1136/bmj.h286.
2. Schols AM, Ferriera IM, Franssen FM, et al. Nutritional assessment and therapy in COPD: a European Respiratory Society statement. Eur Respir J 2014; 44: 1504-1520.
3. Young RP, Hopkins RJ, Eaton TE. Forced expiratory volume in one second: not just a lung function test but a marker of premature death from all causes. Eur Respir J 2007; 30:616-622.
4. Reedy J, Krebs-Smith SM, Miller PE, et al. Higher diet quality is associated with decreased risk of all-cause, cardiovascular disease and cancer mortality among adults. J Nutr 2014; 144: 881-889.
5. Kan H, Stevens J, Heiss, et al. Dietary fibre, lung function, and chronic obstructive pulmonary disease in the Atherosclerosis Risk in Communities Study. Am J Epidemiol 2009; 167: 570-578.
6. Fonseca Wald EL, van den Borst B, Gosker Hr, Schols AMW. Dietary fibre and fatty acids in chronic obstructive pulmonary disease risk and progression: a systematic review. Respirology 2014; 19: 176-184.
7. Young RP, Hopkins RJ. A review of the Hispanic Paradox: time to spill to beans? Eur Respir Rev 2014;23: 439-449.
8. Trompette A, Gollwitzer ES, Yadava K, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and haematopoiesis. Nature Med 2014; 20: 159-168.
9. Young RP, Hopkins RJ, Eaton TE. Pharmacological action of statins: potential utility in COPD. Eur Respir Rev 2009;18: 222-232.
10. Young RP, Hopkins RJ. Primary and secondary prevention of chronic obstructive pulmonary disease: where to next? Am J Respir Crit Care Med 2014; 190: 839-840.
11. Varraso R, Willett WC, Camargo CA. Prospective study of dietary fibre and risk of chronic obstructive pulmonary disease among US women and men. Am J Epidemiol 2010; 171: 776-784.
12. Okubo H, Shaheen SO, Ntani G, et al. Processed meat consumption and lung function: modification by antioxidants and smoking. Eur Respir J 2014; 43: 972-982.
Robert P Young1, Raewyn J Hopkins1 and Corrine Hanson2. 1Schools of Biological Sciences and Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.2 School of Allied Health Professions, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Competing interests: No competing interests
Re: Alternate Healthy Eating Index 2010 and risk of chronic obstructive pulmonary disease among US women and men: prospective study
Varraso, et al. (2015) found that a healthier diet (Alternate Healthy Eating Index 2010) was associated with a lower risk of COPD (1). I found Varraso et al.’s (2015) study fascinating, especially since in my work experience in a nursing home I have seen the toll that COPD takes on individuals and the need to minimize the risk. I found that this study also brought to mind the impact that the environment has on the epigenome. Smoking appears to influence disease risk by its effect on the epigenome (2, 3, 4). It has been speculated that smoking might influence COPD risk in part through epigenetic mechanisms (2, 5). Diet influences the epigenome (6, 7). Dietary components might nudge the epigeome either directly or indirectly through their impact on the gut ecosystem. Whole plant foods, including produce and whole grains, contain phytochemcials that are believed to play roles in epigenetic maintenance (8, 9, 10, 11). Whole plant foods are also important for maintaining a healthy, diverse gut ecosystem (12, 13). In contrast, an overly processed, sugary diet is believed to cause an imbalanced gut ecosystem (13). The gut ecosystem influences the epigenome through chemical signaling which may influence chronic disease risk (14, 15, 16). Thus it seems plausible that diet might influence COPD risk in part through epigenetic mechanisms.
About the author: www.CeliaMRoss.com
(1) Varraso R, Chiuve SE, Fung TT, Barr RG, Hu FB, Willett WC, Camargo CA. Alternate Healthy Eating Index 2010 and risk of chronic obstructive pulmonary disease among US women and men: prospective study. BMJ. 2015 Feb 3;350:h286.
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Competing interests: I write about health issues.