Introduction
Chronic Obstructive Pulmonary Disease (COPD) is a prevalent, preventable, and manageable condition marked by persistent and progressive airflow limitation due to an enhanced inflammatory response in the airways and lungs from exposure to harmful particles or gases.1 As reported in the Global Burden of Disease Study 2019, COPD ranks as the third leading cause of death globally, following ischemic heart disease and stroke.2 In the United States, it significantly contributes to morbidity and mortality, affecting an estimated 16 million adults, though underdiagnosis suggests higher actual numbers.3 Globally, COPD prevalence is around 10.3%based on the Global Initiative for Chronic Obstructive Lung Disease criteria, equating to approximately 391.9 million cases among individuals aged 30 to 79 years.4 The disease’s economic impact is staggering, with annual direct costs exceeding $32 billion in the US alone, compounded by indirect costs from lost productivity and caregiver burdens.5 COPD pathogenesis involves environmental factors, genetic predisposition, and inflammatory processes, characterized by chronic inflammation in the airways and lung parenchyma. This leads to structural changes such as airway remodeling, emphysema, and increased mucus production, driven by immune cells like neutrophils, macrophages, and T lymphocytes, which release pro-inflammatory cytokines and mediators contributing to tissue damage and airflow obstruction.
Recent research underscores the critical impact of diet on COPD pathogenesis and progression.6 The relationship between diet and malnutrition in COPD patients is a critical. Malnutrition is a prevalent yet frequently overlooked comorbidity in patients with COPD, with dietary inadequacies playing a central role in its pathogenesis. Studies indicate that approximately 17–55% of COPD patients exhibit malnutrition, characterized by insufficient energy and protein intake, weight loss, and reduced fat-free mass, which exacerbates disease severity and functional decline.7 Systemic inflammation, driven by cytokines such as TNF-α, and elevated resting energy expenditure (REE) contribute to a catabolic state, further compromising nutritional status despite adequate food consumption.8 For instance, malnourished COPD patients demonstrate significantly lower spirometric values (eg, FEV1 and FVC) and diminished exercise capacity, as evidenced by reduced 6-minute walk distances and peak oxygen uptake.9 Notably, protein-calorie malnutrition correlates with respiratory muscle wasting, impaired diaphragm contractility, and increased dyspnea, as measured by the modified Medical Research Council (mMRC) scale.10 In summary, dietary choices may result in inadequate nutrition for patients with COPD, and malnutrition can affect COPD-related inflammation, with certain patterns either worsening or alleviating the disease. A diet high in meat consumption, saturated fats, and refined carbohydrates is linked to a higher COPD risk, while a diet rich in fruits, vegetables, and whole grains, which contain antioxidants and anti-inflammatory agents, may offer protective benefits. Antioxidants like vitamins A, C, E, and carotenoids are crucial in reducing oxidative stress, a key factor in COPD, and are associated with better lung function and lower COPD risk.11 Studies show that higher carotenoid intake correlates with reduced COPD incidence, highlighting the role of dietary antioxidants in mitigating lung oxidative damage.12 Additionally, dietary fiber, which is fermented into anti-inflammatory short-chain fatty acids by gut microbiota, is linked to improved lung health and reduced COPD risk. This emphasizes the significance of a balanced diet in managing and potentially preventing COPD.13
The Dietary Inflammatory Index (DII) evaluates the inflammatory potential of a diet by assigning inflammatory weights to various food items and nutrients based on their association with inflammatory biomarkers.14 This scoring system categorizes diets from anti-inflammatory to pro-inflammatory, offering insights into dietary influences on health outcomes, particularly chronic diseases like cardiovascular disease, diabetes, asthma, COPD, and cancer.11,15–18 There is an association between higher DII scores and a heightened risk of early COPD along with reduced lung function.19 The association between diet, inflammation, and COPD is recognized; yet, there remains a scarcity of data regarding the specific role of dietary inflammation, as measured by the DII, in influencing COPD in real-world contexts. The objective of this research is to investigate this relationship by utilizing data from the National Health and Nutrition Examination Survey (NHANES) to improve comprehension and guide dietary prevention strategies for COPD.
Materials and Methods
Data Sources
The NHANES evaluates the health and nutritional status of the US civilian noninstitutionalized population. It covers topics like chronic diseases, dietary intake, physical activity, and health behaviors. Participants undergo standardized physical exams in mobile centers, where trained technicians measure health metrics such as height, weight, blood pressure, and conduct laboratory tests. According to the Ethical Review Methods for Life Science and Medical Research Involving Human Participants, Article 32 exempts certain research from requiring ethical approval under specific conditions. Research utilizing legally obtained public data or data derived from non-intrusive observation of public behavior does not require ethical approval.20 Our study complies with exemption conditions by using legally obtained public data and anonymized informational data, ensuring no interference with public behavior. The study’s design, data gathering, and analysis adhered strictly to the STROBE guidelines, guaranteeing methodological rigor and ethical compliance. In addition, the study protocols were sanctioned by the Institutional Review Board of the National Center for Health Statistics (NCHS).21 Since the study relies on publicly accessible data, no patient consent or hospital ethics approval was required, as the data is de-identified and meets exemption criteria for informed consent and ethical approval.
The DII scores data were solely obtained from NHANES cycles between 1999 and 2018, targeting adults aged 18 to 80. Conversely, data on COPD outcomes were solely accessible from the NHANES cycles carried out from 2013 to 2018. In our study, we used NHANES data that is publicly available, sourced from surveys carried out in 2013–2014, 2015–2016, and 2017–2018. A total of 29,400 people participated in these extensive surveys, offering crucial demographic details. We initially excluded 2247 individuals without DII data, which resulted in a group of 27,153 participants aged 18 to 79 years with available DII information. Following this, 12,372 participants lacking COPD data were excluded, along with those missing information on 6185 covariates. Once these exclusions were made, our final analysis sample was composed of 8596 subjects, including 4450 males and 4146 females. A detailed study flowchart illustrating this process is provided in Figure 1.
|
Figure 1 Flowchart of participants selection. Abbreviations: NHANES, National Health and Nutrition Examination Survey.
|
Measurement of DII
Between 1999 and 2018, participants in NHANES provided comprehensive dietary data through two meticulously designed rounds of validated 24-hour dietary recall surveys. These surveys established a robust framework for evaluating individuals’ dietary intake over the specified period. To investigate the inflammatory potential associated with various dietary patterns among participants, researchers employed the DII. The methodology for constructing and validating the DII has been thoroughly addressed in previous studies, ensuring that the index is both reliable and comprehensive.22 In this research, a total of 28 different dietary components were included in the DII calculation, offering a multifaceted view of dietary influences on inflammation. This extensive list encompasses essential macronutrients such as carbohydrates, proteins, total fats, and alcohol, as well as dietary fiber and cholesterol. Notably, the assessment also accounted for different types of fatty acids, including saturated, monounsaturated, and polyunsaturated fatty acids, alongside specific fatty acid profiles like n-3 and n-6. Vitamins were also represented in the analysis, incorporating vital nutrients such as vitamins A, B1 (thiamine), B2, B6, B12, C, D, and E, and various minerals, including iron, magnesium, zinc, selenium, folate, and carotenoids, as well as caffeine and overall energy intake, thereby providing a comprehensive assessment of dietary contributions to inflammation.23
COPD Outcomes
Based on prior research, a self-reported diagnosis of COPD was established by a physician and includes conditions such as chronic bronchitis and emphysema, in addition to COPD itself.24,25 Participants were classified as having COPD through a composite assessment of three self-reported items from a COPD questionnaire administered during individual interviews. The questions posed were: Has a physician ever diagnosed you with chronic bronchitis? Have you ever been diagnosed with emphysema by a physician? Has a healthcare provider ever diagnosed you with COPD?Respondents affirming any of these questions were classified as having COPD, whereas those who did not were categorized as non-COPD.
Covariates Assessment
Previous research26,27 and clinical assessments have identified confounding factors including age, gender, ethnicity, marital status, education level, and poverty income ratio(PIR), along with alcohol consumption, smoking behaviors, levels of physical activity, cardiovascular conditions(CVD), hypertension, cancer, and diabetes mellitus (DM). Information was gathered through standardized questionnaires during family interviews. Ethnicity data was self-reported and categorized as non-Hispanic white, non-Hispanic black, Mexican American, and other racial groups. Marital status was classified as married, never married, living with a partner, or other statuses, which encompass widowed, divorced, or separated. Educational attainment was divided into three levels. Education levels were classified as under high school, high school, and above high school. Family income was divided into three categories according to the family poverty income ratio. Income levels were categorized as low (≤1.3), medium (>1.3 to 3.5), and high (>3.5). Individuals who did not smoke were defined as those who had never engaged in smoking or had smoked fewer than 100 cigarettes in their lifetime. Former smokers were classified as individuals who had consumed at least 100 cigarettes during their lifetime but had since ceased smoking. Conversely, current smokers were defined as those who had smoked a minimum of 100 cigarettes and continued to do so.28 The classification of alcohol consumption included non-drinkers, light to moderate drinkers (up to 2 drinks per day for men and up to 1 drink per day for women), and heavy drinkers (more than 2 drinks per day for men and more than 1 drink per day for women).29 Physical activity was classified into two categories. Individuals are categorized as insufficiently active if they engage in 1 to 5 moderate or 1 to 3 vigorous leisure activities weekly, while those exceeding these levels are considered active.30 Cardiovascular disease (CVD) encompasses conditions such as heart failure, coronary artery disease, angina, heart attacks, and cerebrovascular accidents.26 For more information on these factors, please visit the NHANES website.
Statistical Analyses
Sample weights were applied in all analyses due to NHANES’s complex survey design. For continuous variables, the median and interquartile range (IQR) were used, and categorical variables were represented by unweighted frequencies and weighted percentages. Dietary Inflammatory Index(DII)scores were divided into four categories, with the highest group (Q4) indicating diets with the greatest pro-inflammatory potential, and the lowest quartile (Q1) indicating diets with anti-inflammatory properties. Differences among groups were assessed using the weighted chi-square test or Kruskal–Wallis H-test. The association between DII scores and COPD was examined using weighted logistic regression models, calculating odds ratios (ORs) and 95%confidence intervals (CIs) for each DII quartile, with the lowest quartile as the reference. A restricted cubic spline analysis illustrated the potential non-linear relationship between COPD and DII. The initial model was unadjusted, Model 1 adjusted for age, sex, race or ethnicity, marital status, education level, and poverty income ratio, while Model 2 further adjusted for BMI group, smoking status, drinking status, physical activity, hypertension, diabetes, cancer, and cardiovascular disease (CVD). Statistical interaction tests were conducted to verify the reliability of observed changes. Analyses were performed using R software version 4.4.0, with two-sided p-values below 0.05 considered statistically significant.
Study Participants and Baseline Characteristics
The baseline characteristics of the individuals are shown in Table 1. A total of 8596 adults were enrolled in our study, comprising 4450 males (51.77%) and 4146 females (48.23%). Among these participants, 691 individuals (8.04%) suffered from COPD. The COPD group consisted of older individuals, mainly Non-Hispanic White, who were less often married, had lower incomes, and engaged less in physical activities compared to those without COPD. They exhibited a higher likelihood of being current smokers and a greater prevalence of cardiovascular disease, hypertension, diabetes, and cancer. Participants with COPD generally exhibited higher DII scores compared to those without COPD. Supplementary Table S1 presents the characteristics of subjects categorized by DII score quartiles. An elevated DII score correlated with increased probabilities of being female, a current smoker, Non-Hispanic Black, never married, having reduced physical activity, and possessing lower income. Additionally, participants with elevated DII scores exhibited lower educational levels. Moreover, individuals in the highest inflammation quartile (T4) demonstrated an increased likelihood of having COPD.
 |
Table 1 The Baseline Characteristics of Participants Sourced From the NHANES Database
|
Association of DII with COPD
We conducted a multivariable logistic regression analysis to explore the relationship between DII and COPD (Table 2). Both the unadjusted and multivariate-adjusted logistic regression models demonstrated a positive association, indicating that an increase in DII is correlated with a higher likelihood of developing COPD. In the final model (Model 3), which accounted for all covariates, a one-unit increase in DII, treated as a continuous variable, was associated with a 10%increase in the risk of developing COPD (OR:1.05, 95% CI:1.01–1.11; P=0.007). When DII was categorized into quartiles, the odds ratios with 95%confidence intervals for COPD across the quartiles were 1.10 (0.82, 1.48), 1.34 (1.01, 1.77), and 1.34 (1.01, 1.77), respectively, after adjusting for all covariates in Model 3. Furthermore, the restricted cubic spline model revealed a linear relationship between DII and COPD (P for nonlinearity=0.618) (Figure 2).
 |
Table 2 Association Between the Dietary Inflammatory Index and COPD in the Multiple Regression Model
|
 |
Figure 2 Restricted spline curve for the association between DII and COPD. Abbreviations: DII, Dietary Inflammatory Index; COPD, Chronic Obstructive Pulmonary Disease.
|
Subgroup Analysis
This study performed stratified and interaction analyses to assess the reliability of the association between the DII and COPD incidence across different subgroups. Table 3 illustrates that the subgroup analysis revealed differing associations between DII scores and COPD; however, a predominantly positive correlation was observed in most categories. The interaction test results revealed that cancer status significantly modified the relationship between DII scores and COPD (P for interaction<0.05).
 |
Table 3 Stratified Analysis of the Associations Between DII and COPD
|
Discussion
This is the first study to explore the relationship between the DII and COPD in a large group of adults from the general population. Our analysis identified a strong positive correlation between DII and COPD prevalence, persisting after covariate adjustments. After extensive multivariable adjustments, a statistically significant association was observed. Compared to individuals in the lowest DII quartile (Q1), those in the highest DII quartile (Q4) exhibited a significantly increased OR of 1.34 (95% CI 1.01, 1.77, P<0.001) for COPD. A linear positive relationship was identified between DII and COPD, highlighting the influence of pro-inflammatory diets on heightened COPD risk. Furthermore, our subgroup analyses consistently indicated a strong association between DII and COPD. These findings indicate that DII could be an important marker for COPD. An anti-inflammatory diet for patients with COPD includes fruits rich in antioxidants, such as berries and oranges, as well as natural antioxidant and anti-inflammatory substances.31 The diet may also incorporate vitamin or probiotic supplements, vegetables like spinach and kale, whole grains such as oats and brown rice, and fatty fish high in omega-3 fatty acids, including salmon and mackerel.32 Additionally, nuts and seeds, such as almonds and flaxseeds, provide essential nutrients.33 This dietary approach offers crucial evidence for developing dietary guidelines aimed at improving outcomes for COPD patients.
Limited epidemiological research has investigated the link between DII and COPD. A prior study involving 3962 participants aged 20 to 49 demonstrated that higher DII scores are significantly linked to reduced lung function, particularly affecting Forced Expiratory Volume in one second (FEV1) and Forced Vital Capacity (FVC). An increase in the DII score was associated with a reduction in FEV1 between 0.43 L and 0.58 L, indicating that dietary inflammation might play a role in the decline of lung function in early COPD cases.34 Another study suggested that higher DII scores were positively correlated with lower lung function, with each unit increase in DII associated with a decrease in FEV1 by approximately 3.44 units. This also suggests that a diet high in inflammatory potential may lead to further airway obstruction and respiratory symptoms thereby worsening airflow restriction.35 In a separate analysis involving 121 COPD patients. The study revealed that as the severity of COPD increased, the quality of diet, as measured by the DII, was inversely related to lung function parameters.36 Specifically, patients with more pro-inflammatory dietary patterns exhibited poorer lung function outcomes, emphasizing the importance of dietary interventions in managing COPD.
Epidemiologic and clinical studies on the DII and lung diseases, particularly COPD, are limited. However, experimental research suggests that DII may impact lung health by influencing chronic inflammation, oxidative stress, and related factors. Chronic inflammation is crucial in COPD development, and dietary factors can modulate these inflammatory states. For instance, certain foods and dietary components can either exacerbate or alleviate inflammation, impacting the overall inflammatory burden on the body. The DII measures the inflammatory potential of a person’s diet and is associated with inflammatory markers like C-reactive protein and cytokines, including IL-6 and TNF-α.37 These markers are crucial in the inflammatory processes of COPD, with oxidative stress also playing a key role in its pathogenesis.12 The disease is linked to an imbalance between reactive oxygen species production and the body’s capacity to detoxify these intermediates or repair the damage. Diets high in antioxidants, such as those rich in fruits and vegetables, may help mitigate oxidative stress and its detrimental effects on lung function. Conversely, a pro-inflammatory diet, which is often low in these protective nutrients, may exacerbate oxidative stress and contribute to the progression of COPD.38 In addition to inflammation and oxidative stress, vascular resistance is also a critical aspect of COPD pathophysiology. Chronic inflammation can lead to vascular remodeling and increased vascular resistance, which further complicates the respiratory function in COPD patients. The DII may influence these vascular changes through its effects on systemic inflammation and oxidative stress, thereby impacting pulmonary vascular resistance and overall lung health.18 Overall, the association between DII and COPD emphasizes the potential of dietary changes to impact chronic inflammation, oxidative stress, and vascular resistance, key factors in the disease’s pathogenesis.
This research possesses significant strengths. Firstly, it represents the first exploration of the link between DII an COPD in a representative population within the United States. Secondly, a thorough examination of measurement techniques and protocols was conducted utilizing the NHANES database. Thirdly, we accounted for potential confounders and formulated robust conclusions across various subgroups. Nonetheless, our investigation encountered certain limitations. Our study has limitations. To begin with, the retrospective cohort design presents challenges in fully mitigating confounding bias and establishing cause-and-effect relationships. Secondly, using participants’memories for dietary assessments can lead to recall bias, and any alterations in eating habits during interviews might have been overlooked. Additionally, due to limited data availability, the evaluation of DII was confined to 28 of the originally suggested 45 dietary parameters, potentially affecting the precision of assessing inflammatory potential. Furthermore, the absence of pulmonary function data led to their exclusion as confounding variables, while self-reported COPD may introduce potential misclassification bias into our analysis. Finally, this study did not evaluate specific nutritional elements, particularly the relationship between vitamin D, vitamin C, and COPD. Although a statistically significant correlation exists between the DII) and COPD, the limited sample size and unidentified confounding factors result in a minimal risk difference, which may limit its clinical significance. As a result, upcoming prospective studies should target larger sample sizes to improve the applicability and significance of the results while exploring the causal link between DII and COPD outcomes further. Residual or unidentified confounding effects may persist in observational research. To delve deeper into the causal association between dietary inflammation and COPD outcomes, future studies need to incorporate thorough confounder adjustments, improved dietary assessments, and additional DII parameters.
Conclusion
Our study concludes that a pro-inflammatory diet is significantly linked to an increased risk of COPD in the United States. These findings could provide important insights for future studies focused on highlighting the significance of dietary health, especially for those adhering to pro-inflammatory diets. We advise individuals with these dietary patterns to enhance their consumption of anti-inflammatory foods to lower the risk of COPD.
Data Sharing Statement
This study’s datasets are accessible in the NHANES database (https://www.cdc.gov/nchs/nhanes/index.htm).
Consent for Publication
All authors have read this manuscript and consent to publish it.
Acknowledgments
The authors thank all the participants, investigators, and consortia who contributed to this study.
Author Contributions
Zhi Jian Luo is the first author for this study. All authors significantly contributed to the work, including conception, study design, execution, data acquisition, analysis, and interpretation, as well as drafting, revising, or critically reviewing the article. They approved the final version for publication and agreed to be accountable for all aspects of the work involved in data acquisition, analysis, interpretation, or execution; participated in drafting, revising, or conducted a critical review of the article, approved the final version for publication, consented to the journal submission, and accepted responsibility for all aspects of the work.
Disclosure
The authors have no relevant financial or non-financial interests to disclose for this work.
References
1. Li M, Hanxiang C, Na Z, et al. Burden of COPD in China and the global from 1990 to 2019: a systematic analysis for the global burden of disease study 2019. BMJ Open Respir Res. 2023;10(1). doi:10.1136/bmjresp-2023-001698
2. Lei J, Huang K, Wu S, et al. Heterogeneities and impact profiles of early chronic obstructive pulmonary disease status: findings from the China pulmonary health study. Lancet Reg Health West Pac. 2024;45:101021. doi:10.1016/j.lanwpc.2024.101021
3. Dotan Y, So JY, Kim V. Chronic bronchitis: where are we now? Chronic Obstr Pulm Dis. 2019;6(2):178–192. doi:10.15326/jcopdf.6.2.2018.0151
4. Adeloye D, Song P, Zhu Y, et al. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease(COPD)in 2019: a systematic review and modelling analysis. Lancet Respir Med. 2022;10(5):447–458. doi:10.1016/S2213-2600(21)00511-7
5. Iheanacho I, Zhang S, King D, et al. Economic burden of chronic obstructive pulmonary disease (COPD): a systematic literature review. Int J Chron Obstruct Pulmon Dis. 2020;15:439–460. doi:10.2147/COPD.S234942
6. Cervilha DAB, Ito JT, Lourenço JD, et al. The Th17/Treg cytokine imbalance in chronic obstructive pulmonary disease exacerbation in an animal model of cigarette smoke exposure and lipopolysaccharide challenge association. Sci Rep. 2019;9(1):1921. doi:10.1038/s41598-019-38600-z
7. Mete B, Pehlivan E, Gülbaş G, et al. Prevalence of malnutrition in COPD and its relationship with the parameters related to disease severity. Int J Chron Obstruct Pulmon Dis. 2018;13:3307–3312. doi:10.2147/COPD.S179609
8. Ogan N, Yıldırım F, Süzen B, et al. Does nutritional risk screening 2002 correlate with the dyspnea status of patients with GOLD stage C-D chronic obstructive pulmonary disease? Turk Thorac J. 2020;21(1):49–53. doi:10.5152/TurkThoracJ.2019.180194
9. Shen X, Qian R, Wei Y, et al. Prediction model and assessment of malnutrition in patients with stable chronic obstructive pulmonary disease. Sci Rep. 2024;14(1):6508. doi:10.1038/s41598-024-56747-2
10. Khan NA, Kumar N, Daga MK. Effect of dietary supplementation on body composition, pulmonary function and health-related quality of life in patients with stable COPD. Tanaffos. 2016;15(4):225–235.
11. Chen C, Yang T, Wang C. The dietary inflammatory index and early COPD: results from the national health and nutrition examination survey. Nutrients. 2022;14(14). doi:10.3390/nu14142841
12. Liu Z, Li J, Chen T, et al. Association between dietary antioxidant levels and chronic obstructive pulmonary disease: a mediation analysis of inflammatory factors. Front Immunol. 2023;14:1310399. doi:10.3389/fimmu.2023.1310399
13. Shin MK, Kwak SH, Park Y, et al. Association between dietary patterns and chronic obstructive pulmonary disease in Korean adults: the Korean genome and epidemiology study. Nutrients. 2021;13(12):4348. doi:10.3390/nu13124348
14. Shivappa N, Steck SE, Hurley TG, Hussey JR, Hebert JR. Designing and developing a literature-derived, population-based dietary inflammatory index. Public Health Nutr. 2014;17(8):1689–1696. doi:10.1017/S1368980013002115
15. Tan J, Liu N, Sun P, et al. A proinflammatory diet may increase mortality risk in patients with diabetes mellitus. Nutrients. 2022;14(10):2011. doi:10.3390/nu14102011
16. Ji M, Hong X, Chen M, et al. Dietary inflammatory index and cardiovascular risk and mortality: a meta-analysis of cohort studies. Medicine. 2020;99(20):e20303. doi:10.1097/MD.0000000000020303
17. Ugai T, Liu L, Tabung FK, et al. Prognostic role of inflammatory diets in colorectal cancer overall and in strata of tumor-infiltrating lymphocyte levels. Clin Transl Med. 2022;12(11):e1114. doi:10.1002/ctm2.1114
18. Wang S, Wang Y, Hu X, et al. Association between dietary inflammation index and asthma COPD overlap. Sci Rep. 2024;14(1):8077. doi:10.1038/s41598-024-58813-1
19. Ingadottir AR, Beck AM, Baldwin C, et al. Two components of the new ESPEN diagnostic criteria for malnutrition are independent predictors of lung function in hospitalized patients with chronic obstructive pulmonary disease(COPD). Clin Nutr. 2018;37(4):1323–1331. doi:10.1016/j.clnu.2017.05.031
20. Brittain S, Ibbett H, de Lange E, et al. Ethical considerations when conservation research involves people. Conserv Biol. 2020;34(4):925–933. doi:10.1111/cobi.13464
21. Centers for Disease Control and Prevention(CDC). National Center for Health Statistics (NCHS). National health and nutrition examination survey data. Hyattsville, MD: US department of health and human services, centers for disease control and prevention. 2021. Available from: https://wwwn.cdc.gov/nchs/nhanes/Default.aspx.
22. Marx W, Veronese N, Kelly JT, et al. The dietary inflammatory index and human health: an umbrella review of meta-analyses of observational studies. Adv Nutr. 2021;12(5):1681–1690. doi:10.1093/advances/nmab037
23. Chang Y, Yu C, Dai X, Sun H, Tang T. Association of dietary inflammatory index and dietary oxidative balance score with gastrointestinal cancers in NHANES 2005-2018. BMC Public Health. 2024;24(1):2760. doi:10.1186/s12889-024-20268-4
24. Huang Q, Yuan Q, Li W, He X, He Q, Deng Z. Dose-response relationship between Life’s Essential 8 score and COPD risk: the NHANES cohort study 2007-2018. Front Med. 2025;12:1446782. doi:10.3389/fmed.2025.1446782
25. Jia S, Chen Q, Huang W, Wang P, Zeng Y. Relationship between systemic immune response index (SIRI) and COPD: a cross-sectional study based on NHANES 2007-2012. Sci Rep. 2025;15(1):7887. doi:10.1038/s41598-025-90947-8
26. Li Q, Chen Y, Yang M, et al. The dietary inflammatory index (DII®)and human papillomavirus infection: a cross-sectional study of US women. BMC Public Health. 2024;24(1):3031. doi:10.1186/s12889-024-20490-0
27. Guan Z, Ma L, Wu C. Association between serum klotho and physical frailty in middle-aged and older adults: finding from the national health and nutrition examination survey. J Am Med Dir Assoc. 2023;24(8):1173–1178.e2. doi:10.1016/j.jamda.2023.02.103
28. Zuo R, Ge Y, Xu J, et al. The association of female reproductive factors with risk of metabolic syndrome in women from NHANES1999–2018. BMC Public Health. 2023:232306. doi:10.1186/s12889-023-17207-0
29. Chen F, Song Y, Li W, Xu H, Dan H, Chen Q. Association between periodontitis and mortality of patients with cardiovascular diseases: a cohort study based on NHANES. J Periodontol. 2024;95(2):175–184. doi:10.1002/JPER.23-0276
30. Yun L, Berry TR, Holt NL, Pelletier LG. Political orientation and public attributions for the causes and solutions of physical inactivity in Canada: implications for policy support. Front Public Health. 2019;7:153. doi:10.3389/fpubh.2019.00153
31. Ilari S, Vitiello L, Russo P, et al. Daily vegetables intake and response to COPD rehabilitation. The role of oxidative stress, inflammation and DNA damage. Nutrients. 2021;13(8):2787. doi:10.3390/nu13082787
32. Kentson M, Leanderson P, Jacobson P, et al. Oxidant status, iron homeostasis, and carotenoid levels of COPD patients with advanced disease and LTOT. Eur Clin Respir J. 2018;5(1):1447221. doi:10.1080/20018525.2018.1447221
33. Zhang C, Yu L, Xiong T, et al. Exploring a potential causal link between dietary intake and chronic obstructive pulmonary disease: a two-sample Mendelian randomization study. Int J Chron Obstruct Pulmon Dis. 2024;19:297–308. doi:10.2147/COPD.S445706
34. Wood LG, Shivappa N, Berthon BS, et al. Dietary inflammatory index is related to asthma risk, lung function and systemic inflammation in asthma. Clin Exp Allergy. 2015;45(1):177–183. doi:10.1111/cea.12323
35. Yazdanpanah L, Paknahad Z, Moosavi AJ, et al. The relationship between different diet quality indices and severity of airflow obstruction among COPD patients. Med J Islam Repub Iran. 2016;30:380. PMID:27493924.
36. Maisonneuve P, Shivappa N, Hébert JR, et al. Dietary inflammatory index and risk of lung cancer and other respiratory conditions among heavy smokers in the COSMOS screening study. Eur J Nutr. 2016;55(3):1069–1079. doi:10.1007/s00394-015-0920-3
37. Shivappa N, Bonaccio M, Hebert JR, et al. Association of proinflammatory diet with low-grade inflammation: results from the Moli-sani study. Nutrition. 2018;54:182–188. doi:10.1016/j.nut.2018.04.004
38. Ramallal R, Toledo E, Martínez-González MA, et al. Dietary inflammatory index and incidence of cardiovascular disease in the SUN cohort. PLoS One. 2015;10(9):e0135221. doi:10.1371/journal.pone.0135221