Furthermore, women may have a different sensitivity to harmful components present in cigarette smoke, and it may be a result of sex-specific pathogenic mechanisms, sex hormones, or different baseline health status of men and women. The study was further limited by an inability to capture AECOPD events treated at non-VA facilities, a lack of spirometry data confirming COPD diagnosis, and an overwhelmingly male population. First, although results from all 8 studies were adjusted for age, gender, smoking status, and other confounders, the effects of residual or unknown confounding factors on the observed findings could not be ruled out completely. Second, the protective effect of FV was observed in all three study designs, but the results of the three study designs were inconsistent in the analysis of fruits and vegetables. Cohort design meets the criteria of temporality and provides stronger evidence for the hypothesis. In the analysis of vegetables, protective effects were found in case-control and cross-sectional design, while cohort design showed an inverse but not significant result.
Baseline characteristics
- Advanced age and cigarette smoking are important risk factors for developing COPD (2, 25, 26).
- In addition, BMI, physical activity, intake of energy, and other confounders also have been adjusted in most studies.
- Standing height and weight were measured by qualified personnel with calibrated tools.
- Subgroup analysis was conducted by study design, continent where the study conducted, gender, and exposure measures.
- The authors also describe a number of potential biologic mechanisms by which alcohol and/or polyphenols might affect lung tissue and increase or decrease the risk of COPD.
Dietary fiber intake was assessed in 1987 and 1997 with a food frequency questionnaire. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Among persons with COPD at high risk of exacerbation, we found no significant relationship between self-reported baseline alcohol intake and subsequent exacerbations. The number of patients reporting heavy alcohol intake was small and further study is needed to determine the effect of heavy alcohol intake on AECOPD risk. SES is defined as a broad concept to reflect social and economic status, which is often measured by income, education and occupation 30.
Study participants
Smoking was defined as three categories—never smoker, former smoker, and current smoker—using self-reported responses to the survey questions about smoking. Never smokers were defined as those who reported smoking fewer than 100 cigarettes in their entire life. Current smokers were defined as those who reported smoking at least 100 cigarettes in their life and were currently smoking every day or some days. Former smokers were defined as those who smoked more than 100 cigarettes during their lifetime but currently did not smoke at all. Linked mortality files provided mortality follow-up data from the month of the interview through December 31, 2019. Mortality information was obtained using a probabilistic match algorithm between the NHIS surveys and death certificate records in the NDI data 38.
Availability of data and materials
All analyses were done to account for the complex, stratified, multistage cluster sampling design of the NHIS by using stratification, clustering, and sample weights in the NHIS data. The baseline characteristics of participants are obtained at the start of survey. To compare baseline characteristics among different groups, we used the χ2 test for categorical variables and analysis variance for continuous variables.
- Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with persistent airflow limitation usually caused by prolonged exposure to noxious gases or particles, particularly cigarette smoke (1, 2).
- Using this method, fiber intake was adjusted for total energy intake to 1600 kcal/day in 1987 and to 1700 kcal/day in 1997 (the mean energy intake in both diet measurements) 20.
- At last, a total of seven articles 9–15 (8 studies) were involved in this meta-analysis.
- It has also been reported that dietary fiber may lower risk of COPD through modulating the innate immune system via the gut–liver–lung axis 13.
Long-term fiber intake
Participants classified as “former unknown frequency drinker,” “current unknown level drinker,” or “drinking status unknown” were not included in this study. Our study strengthens and expands previous evidence that, in addition to smoking cessation, intake of dietary fiber as a modifiable lifestyle factor may reduce the risk of COPD for both ex- and current long-term smokers. Therefore, our results support the recommendation to increase consumption of products high in dietary fiber especially among smokers. Furthermore, these findings indicate the need to conduct intervention studies on the clinical utility of recommending intake of at least 25 g of fiber/day to reduce the risk of COPD among long-term smokers.
Data Availability Statement
CC, KL, KH, DS, and SL conceived and designed the study and contributed to data interpretation. The studies involving human participants were reviewed and approved by the Institutional Review Board of the Asan Medical Center, Seoul, Republic of Korea. Written informed consent for participation was not required for this study in accordance with the national legislation and the institutional requirements. Proportion free from AECOPD for 1 year, according to alcohol consumption pattern.
All NHIS participants aged 18 years and older with sufficient identifying data were eligible for mortality follow-up. To reduce participant disclosure risk, the NCHS developed data-perturbation techniques. Previous studies have confirmed the accuracy of information on mortality in the NDI records 39. Our findings indicate that high fiber intake is a modifiable lifestyle factor which may decrease COPD risk primarily in current and ex-smokers.
All-cause mortality according to alcohol consumptionstatus and NHIS year among NHIS participants in 1997 to2014.Hazards ratios for all-cause and cause-specific mortality according to alcoholconsumption status among NHIS participants in 1997 to 2014. Hazards ratios forall-cause and cause-specific mortality according to alcohol consumptionstatus stratified for sex, age, race/ethnicity and smoking status amongNHIS participants in 1997 to 2014. Our findings align with prior research demonstrating dose-dependent effects of alcohol on cardiac electrophysiology and arrhythmogenic risk. Notably, two large-scale meta-analyses showed a clear association between increasing alcohol consumption and heightened risk of atrial fibrillation 13, 14. These studies support the notion that even moderate alcohol intake can influence cardiac rhythm, and that alcohol consumption and risk of chronic obstructive pulmonary disease: a prospective cohort study of men the risk escalates with higher doses.
Data availability
In China, the dearth of hygienic domestic fuels and inadequate kitchen ventilation may contribute to indoor air pollution, which has been identified as a threat to women with COPD 26. Forum members thought that there are a number of deficiencies in this study that somewhat weaken its conclusions; especially important was the lack of ability to consider the pattern of drinking (regular, moderate versus binge drinking). Still, there is a strong consistency between the results of this study (indicating a “J-shaped” or “U-shaped” curve for alcohol intake and COPD) and results from extensive previous epidemiologic and experimental research.
A likelihood ratio test was used to examine the interaction between long-term fiber intake and smoking status (ever vs. ex-smokers vs. current smokers) on COPD risk. The shape of the association between risk of COPD and long-term total dietary fiber intake was investigated using restricted cubic-splines with three knots (at the 10th, 50th, 90th percentile) 25. (SAS Institute Inc, Cary, NC, USA) and STATA v. 13 (StataCorp, College Station, TX, USA). All P values were two-sided and values ≤ 0.05 were considered statistically significant. Data about food consumption were collected by food frequency questionnaires (FFQs) based on 67 food items in 1987 and 96 food items in 1997. Participants were asked about their average food consumption during the past year based on eight predefined frequency categories, ranging from “never/seldom” to “4 times per day” in 1987, and from “0 times per month” to “3 + times per day” in 1997.
Although the results of this study were basically consistent, these methods may not be sufficient to solve this problem. The findings of cancer mortality may not align with cause-specific cancer outcomes, such as liver cancer, oral cancer, and esophageal cancer. Also, the results related to cancer mortality may differ from the findings related to cancer incidence.
Thus, the protective effects of vegetables on COPD need to be investigated further. Third, the assessment methods of fruit and vegetable consumption were different, which may have a certain impact on the results. In the analysis of vegetables, the pooled result (RR, 0.76; 95% CI, 0.63–0.92) was overestimated by 13.6% due to the use of other questionnaires. Fourth, there were no uniform diagnostic criteria for COPD and no detailed disease information in the included studies. Therefore, the status (Mild, Moderate, Severe) of COPD patients was unclear, and we were unable to perform a pooled analysis. To provide greater diagnostic power than unscaled residuals, the proportional hazards assumption was evaluated by regressing scaled Schoenfeld residuals against survival time, and evidence of rejection of the assumption was not found.
