Individual Foods and Nutrients, Lung Function, and COPD

6.1. Role of Antioxidant and Anti-Inflammatory Foods: Fruits and Vegetables
The dietary quality and the nutritional status of COPD patients as well as the oxidative– inflammatory pathogenic basis of COPD provided the rationale to verify the respiratory effects of antioxidant and anti-inflammatory dietary components. Consistent epidemiologic evidence from cross-sectional [36,38,48–51] and longitudinal studies [42,52–55] reported potential beneficial effects of a high intake of antioxidant nutrients (vitamins and nonvitamins) and of foods rich in antioxidants, mostly fresh, hard fruits and, to a lesser extent, vegetables, on lung function and COPD symptoms [35,36,49–51], decline in lung function [42,49,56], incidence of COPD [52,54,55], and mortality [53].

Two recent large population-based prospective studies in Swedish men [54] and women [55] confirmed the inverse and independent association between high long-term consumption of fruits (in both men and women) and vegetables (only in men) and incidence of COPD (35% lower risk in men, p for trend <0.0001 [54]; 37% lower risk in women, p for trend <0.0001 [55]). These beneficial dietary associations were particularly evident among smokers. Specifically, in the cohort of men (with higher smoking intensity than women), the protective effect was restricted to current and ex-smokers (40% lower risk, p for trend <0.0001, and 34% lower risk, p for trend = 0.001, respectively), mostly benefiting from dietary antioxidants, probably as a result of increased oxidative stress level due to smoking compared with never smoking, and the continued oxidative burden even after smoking cessation [54]. Regarding individual food items, intakes of apples, pears, peppers, and green leafy vegetables were negatively associated with the risk of COPD [54]. Few randomized dietary intervention trials have been conducted. In a small 12-week randomized trial including moderate-to-severe COPD patients complying with an intervention to increase fruit intake, no improvement in airways or systemic inflammation and oxidative stress markers was observed, although the follow-up might have been too short to observe any significant effect [57]. In COPD patients, 1-week supplementation with beetroot juice, a dietary source of nitrates that improves mitochondrial respiration and energy production via nitric oxide formation, increased plasma nitrate levels and decreased diastolic blood pressure (mean difference 4.6 mmHg, 95% CI: 0.1, 9.1, p < 0.05) without any effect on walking capacity, physical activity level, or oxygen consumption of submaximal exercise [58]. However, another randomized trial reported that COPD patients following a diet rich in fruits and vegetables (>1 portion/day) showed an annual increase in FEV1 compared with the control group following a free diet over 3 years (p = 0.03), after adjustment for physical activity, alcohol intake, co-morbidities, and exacerbation frequency [59].
Collectively, these observations suggest fruit and vegetable consumption as an important determinant of pulmonary function and COPD risk. It should be noted that fresh fruit intake may be one component of an overall healthier lifestyle, including less smoking, more physical activity, low consumption of Western foods (e.g., meat), and increased consumption of vegetables [54,55,59], and other not checked nutrients may mediate the observed beneficial effects. Furthermore, assessment of blood, urine or exhaled breath condensate biomarkers of endogenous oxidative stress is generally lacking in most longitudinal studies, thus limiting the possibility to more accurately select subjects more susceptible to antioxidant dietary regimens and to appraise the antioxidant efficacy of tested foods over time.
6.2. Vitamin and Nonvitamin Antioxidants
Plausible mechanisms underlying fruit and vegetable protective effects include their antioxidant and anti-inflammatory activities, as suggested by the epidemiologic association observed between fruit and vegetable consumption and lower markers of oxidative stress and inflammation, and higher levels of antioxidant markers [60,61]. Fruits’ and vegetables’ beneficial effects on respiratory function may be partially contributed by their high content in vitamin and nonvitamin antioxidants. Accordingly, higher dietary intakes of vitamin C, a hydrophilic antioxidant, were associated with higher levels of FEV1 [35,62] and with a lower rate of decline in FEV1 after a 9-year follow-up period [62]. Other studies did not confirm a significant effect of vitamin C dietary intake on lung function (FEV1), its longitudinal decline [49], COPD incidence [52] or mortality [53]. Although not consistently [62], a protective role has also been credited to other vitamins such as vitamin E or tocopherol, a lipid soluble antioxidant acting in synergy with vitamin C and able of breaking lipid peroxidation chain reaction and protecting the lung against oxidative damage [36,53]. Lower serum vitamin E levels have been observed in COPD during exacerbation compared to stable condition [63]. Randomized trials of vitamin E supplementation in clinical populations have, however, reported mixed results, including both protective [64] and no effects [33] on the risk of developing COPD.

Butland et al. [49] found a positive cross-sectional association between higher consumption of hard fruits, such as apples (5 or more apples per week) and lung function (FEV1) (138 mL higher FEV1 for those eating 5 or more apples per week compared with nonconsumers, 95% CI: 58.1, 218.1, p for trend
<0.001), more strongly than soft or citrus fruits and independent of vitamin E and vitamin C intakes. Similarly, Miedema et al. [52] found a stronger inverse association with 25-year incidence of COPD for solid fruits (apples, pears) than for other types of fruits. Other nonvitamin dietary components may therefore exert protective effects. These include the fat-soluble antioxidant carotenoids (lycopene, lutein, zeaxanthin, and the provitamin A carotenoids α-carotene, β-carotene, and β-cryptoxanthin), whose serum and dietary levels have been positively correlated to lung function indicators (FEV1, FVC) [35,42,65]. However, long-term supplementation with β-carotene or α-tocopherol failed to reduce
COPD symptoms in a large cohort of male smokers randomized into the α-tocopherol and β-carotene
Cancer Prevention (ATBC) Study [66]. Notably, strong evidence from randomized controlled trials conducted in heavy smokers and asbestos-exposed workers, i.e., the β-carotene and retinol efficacy trial (CARET) [67] and the abovementioned ATBC study [68], showed that high-dose β-carotene supplements may increase the risk of lung cancer and of death from lung cancer, CVD, and any cause. Contrarily, this harmful effect was not observed among healthy male physicians in the
Physicians’ Health Study in the USA [69]. An interaction of carotenoids with cigarette smoking has been proposed to explain the shifting of carotenoid antioxidant potential into a pro-oxidant detrimental effect on the lung: β-carotene can easily form oxidation products with pro-oxidant effects, especially at high concentrations in the oxidative environment of the smoker’s lung characterized by increased cell oxidative stress and decreased antioxidant defense [70]. Against this background, according to the 2018 report of the World Cancer Research Fund/American Institute for Cancer Research (, β-carotene supplements (and dietary supplements in general) are not recommended for cancer prevention (especially in smokers), while intake of natural micronutrients through diet is advisable. Therefore, caution should be taken, especially in smokers, when considering dietary supplementation with β-carotene.
Other potentially protective dietary factors include polyphenols, the most abundant antioxidants
in human diets naturally present in plant foods, and exhibiting potent anti-inflammatory properties. Polyphenols, including phenolic acids, flavonoids (flavonols, flavones, isoflavones, flavanones, flavanols, and anthocyanidins), stilbenes (resveratrol, etc.), lignans, and secoiridoids, have been reportedly associated with prevention of chronic diseases, including CV and neurodegenerative diseases and cancer, and with the promotion of healthy aging [71]. Beneficial effects on respiratory function have been reported for the flavonoid class of polyphenols: In an earlier Dutch study, the intake of catechins was positively associated with FEV1 (mean difference in FEV1 comparing high vs. low intake of catechins = 130 mL, 95% CI: 101–159, p < 0.05) and negatively associated with all three COPD symptoms (odds ratio (OR) of phlegm, breathlessness and cough, comparing high vs. low intake of catechins = 0.60–0.72, p < 0.001) [50]; concordantly, slower longitudinal decline in lung function was observed with higher intake of anthocyanidins in US elderly men [72], and a beneficial association of dietary intakes of isoflavones as well as of soy, which is a rich food source of isoflavones, with lung function and COPD prevalence was also observed in Japanese adults [73,74]. In a recent randomized trial in COPD patients, supplementation with flavonoids in the form of oligomeric pro-anthocyanidins extracted from grape seeds was effective in improving oxidative stress and lipid profile, but not lung function parameters after 8 weeks [75]. More recent observational findings in a Mediterranean population confirmed protective effects of the intake of various polyphenol classes on pulmonary function parameters [76]. In a cross-sectional study in 267 Spanish COPD patients, dietary intakes of vitamin E as well as vegetables and olive oil, rich in vitamin E and polyphenols, have been shown to be inversely correlated with serum markers of oxidative stress, especially in current smokers [77]. In an Asian population-based cross sectional study, a diet rich in the potent antioxidant and anti-inflammatory turmeric-derived polyphenol curcumin was significantly and independently associated with improved lung function measures, and smokers with the highest curcumins intake

had levels of lung function greater than smokers not consuming curcumins and similar to those of nonsmokers, supporting the antioxidant and anti-inflammatory dietary hypothesis [78].
6.3. Minerals
Among micronutrients, cross-sectional studies have found deficient intake of some minerals in COPD patients. Indeed, dietary intakes and serum levels of calcium, magnesium, and selenium were found to be below the recommended values in older, underweight patients with severe COPD [79]. Lower intakes of calcium and zinc were observed in elderly COPD patients compared with non-COPD subjects [45]. Some minerals have been studied in relation to lung function and COPD risk and symptoms. A case-control study in Japanese adults found a positive association between intake of calcium, phosphorus, iron, potassium, and selenium and lung function measures (e.g., FEV1), and an inverse association between dietary calcium intake and COPD risk (35% reduction) [80]. FEV1 was independently and positively associated with serum levels of selenium, normalized calcium, chloride, and iron, and was inversely related to potassium and sodium in the general population [43]. Other cross-sectional studies confirmed the association between serum levels of selenium as well as copper and higher lung function [81]. A randomized placebo-controlled trial reported that selenium supplementation (200 µg/d L-selenomethionine), either alone or in combination with vitamin E (400 IU/d all rac-α-tocopheryl acetate), did not affect decline in FEV1 or FEF25–75, a marker of airflow, but attenuated decline in FEF25–75 (by 59 mL/second/year) in current smokers, who may benefit most from selenium supplementation due to its potent antioxidant properties linked to the glutathione peroxidase activity [82].
Early population-based studies reported a strong association between magnesium intake and lung function, airway hyper-responsiveness, and wheeze [83], although this result was not consistently found [49]. More recently, in a general UK population cohort intake of magnesium was cross-sectionally related to higher FEV1 (a 100 mg/day higher magnesium intake was associated with a 52.9 ml higher FEV1 (95% CI, 9.6–96.2)), but no relationship between intake of magnesium and longitudinal decline in FEV1 was seen [62]. Similar results were recently obtained by Leng et al. [84] in New Mexico white smokers. Magnesium may play a beneficial role in respiratory function and COPD, through its protective effects against inflammation and bronchoconstriction [85]. Although the limited evidence suggests protective effects of some minerals on lung function and COPD, mostly for those endowed with antioxidant and anti-inflammatory properties, further prospective studies are warranted.
6.4. Wholegrains and Fibers
Among dietary factors largely investigated, mostly in relation to CVD and cancer, research has also focused on wholegrains. Observational studies reported an independent beneficial effect of a high wholegrain intake on lung function [51,86], and against mortality from chronic respiratory disease [87]. Wholegrains are rich in phenolic acids, flavonoids, phytic acid, vitamin E, selenium, and essential fatty acids, which may additively or synergistically contribute to wholegrain documented beneficial effect on respiratory as well as nonrespiratory diseases.
Part of the protective action of wholegrains as well as of fruits and vegetables is attributable to the antioxidant and anti-inflammatory properties of their fiber content [88]. Indeed, epidemiological data indicated that fiber intake is associated with lower serum levels of C-reactive protein and cytokines (IL-6, TNF-α) and higher level of adiponectin, an insulin-sensitizing adipocytokine with anti-inflammatory properties [89]. In line with these beneficial properties, cross-sectional and longitudinal studies found a negative and independent association between total fiber intake and lung function decline, and COPD incidence and prevalence [90–92]. Indeed, higher dietary intake of total fiber reduced by about 40% the risk of COPD in large prospective studies [91,92]. Considering fiber types (cereal, fruit, vegetable), the beneficial association was observed mostly for cereal fiber intake mainly in current smokers and ex-smokers, but evidence exists also for fruit and vegetable fiber intake [91,92].

6.5. Alcohol and Wine
Other significant associations with respiratory health have been documented in the general population for intake of alcohol and wine. Previous epidemiologic studies found that subjects with low alcohol consumption (1–30 g/day) had higher levels of FEV1, lower prevalence of COPD symptoms [51], and a decreased risk of COPD compared to nonconsumers [52]. By contrast, heavy alcohol intake, as assessed by both dietary and serum biomarker measurements, was shown to have negative effects on lung function, additive to that of smoking [93]. Among the different alcohol sources, only wine intake (>7.4 g/day) was found to be positively associated with FEV1 in the general population [94], as well as with a lower risk of airway obstruction, defined as an abnormally low FEV1/FVC ratio, predominantly in smokers [95]. Beyond direct protective effects of alcohol as previously reported [96], putative candidates accounting for the observed beneficial effect of wine are flavonoids [50], as well as the stilbene resveratrol [95], both associated with improved measures of lung function. Congruently, resveratrol has been reported to exert anti-inflammatory properties in airway epithelial cells [97], alveolar macrophages derived from COPD patients [98], and airways smooth muscle cells [99], and the flavonol quercetin has been shown to attenuate rhinovirus-induced lung inflammation and emphysema progression in a mice model of COPD [100].
Interestingly, the independent beneficial effects of a favorable intake of fruits (>180 g/day), wholegrains (>45 g/day), and alcohol (1–30 g/day) on FEV1 and COPD symptoms were additive (favorable vs. unfavorable intake, 139 mL higher FEV1 and COPD symptoms prevalence OR = 0.44, p < 0.001) [51], suggesting important interaction among nutrients and food groups. Moreover, findings from the ECLIPSE study in COPD subjects demonstrated that recent consumption of “healthy” foods, such as fruits (grapefruit and bananas), fish, tea, dairy products, and alcohol, was associated with higher lung function and less decline over time, less emphysema and emphysema progression, greater 6-minute walk and St. George’s Respiratory Questionnaire (SGRQ) scores, and lower levels of inflammatory markers (C-reactive protein, white blood cells, surfactant protein D, total neutrophils) [101]. These data extend the role for dietary intakes to phenotypic features of COPD patients.
6.6. Vitamin D
Limited evidence also supports a direct correlation between vitamin D levels, which mainly depend on sun exposure in addition to diet, and lung function, COPD incidence, symptoms, severity and progression [102–104]. Genetic variants in the vitamin D-binding protein associated with lower plasma vitamin D levels have also been linked to COPD risk [105]. Mechanistic studies support a role for vitamin D other than calcemic effects and in particular in normal growth and development of the lung as well as in immune responses and COPD progression. Vitamin D supplementation trials to prevent COPD exacerbation reported conflicting results but, collectively, pointed to a benefit only in patients with low baseline vitamin D levels (i.e., levels of active metabolite 25-hydroxyvitamin D
<25 nmol/L) [106]. Although further studies are needed, taking into account the highly prevalent osteoporosis and risk of falls in COPD patients and also the supposed beneficial effects of vitamin D beyond bone health, screening for vitamin D deficiency (25-hydroxyvitamin D <50 nmol/L) may be important in COPD patients.
6.7. Coffee and Its Components
Given its widespread consumption, interest has been growing around the potential role of coffee in respiratory health. Findings from literature reviews point to an association between regular (not decaffeinated) coffee intake and improved lung function and reduced mortality from respiratory disease, but not COPD [107], with contributory roles for its constituents, caffeine (bronchodilator, anti-inflammatory) and polyphenols (antioxidant, anti-inflammatory). Smoking is a major confounder in these studies because it may accelerate the hepatic metabolism and clearance of caffeine or may

dilute or dampen the beneficial effects of coffee through its potent pro-oxidant and pro-inflammatory action [107].
6.8. Role of Fish and n-3 Polyunsaturated Fatty Acids
α-Linolenic acid (ALA, C18:3) and its long-chain derivatives eicosapentaenoic acid (EPA, C20:5) and docosahexaenoic acid (DHA, C22:6) are polyunsaturated fatty acids (PUFA) of the n-3 (omega-3) family. Due to the low efficiency of endogenous synthesis from precursors, they are considered nutritionally essential and depend on exogenous source, mainly seafood (fatty fish). n-3 PUFAs and fish display potent anti-inflammatory properties with beneficial effects and, in most cases, clinical applications in several chronic inflammatory diseases, including CVD, cancer, rheumatoid arthritis, and diabetes [108]. Opposite effects have been described for n-6 PUFAs, including linoleic acid (LA, C18:2) and its long-chain derivative arachidonic acid (AA, C20:4), mainly found in vegetable oils (soybean, corn, and sunflower oils), grain-fed animals, dairy, and eggs. Indeed, metabolism of long-chain n-6 PUFA produces eicosanoids (such as thromboxane(TX) A2, prostaglandin(PG) E2 and leukotriene(LT) B4) which are more potent mediators of inflammation, thrombosis, and vaso- and bronco-constriction than similar products derived from n-3 PUFAs (PGs of the 3-series and LTs of the 5-series) [109]. Some EPA and DHA metabolites via cytochrome P450 enzymes, which are highly expressed in the lungs, are potent vasodilators and bronchodilators and show anti-inflammatory properties. Other metabolites of long-chain n-3 PUFAs include the inflammation-resolving eicosanoids resolvins and protectins, which act to remove inflammatory mediators and promote healing.
Increasing the content of n-3 PUFA in the diet causes a partial substitution of the n-6 PUFA in the cell membranes and competition for the metabolizing enzymes, thus favoring the synthesis of generally less biologically active eicosanoids. In addition to lipid metabolites, n-3 PUFA anti-inflammatory mechanisms also include the direct modulation of inflammatory gene expression (adhesion molecules, cytokines, matrix degrading enzymes, cyclooxygenase-2) via the regulation of nuclear transcription factors, mainly the oxidative stress-sensitive pro-inflammatory NF-κB [109], which has also been involved in the pathogenesis of lung inflammation [24].
The secular trend of dietary shift to a more Westernized pattern and the following increased consumption of n-6 PUFAs and decreased consumption of n-3 PUFAs is thought to have contributed to the rise in chronic inflammatory disease [108]. Given the role of inflammation in COPD and the reported benefits of long-chain n-3 PUFAs in many inflammatory diseases, studies have been conducted to verify the ability of dietary PUFAs to also modulate COPD (prevalence, severity, and health outcomes). However, as underlined in a recent systematic review [110], data are conflicting. Some earlier observational studies suggest benefits from increased consumption of n-3 PUFA-rich foods, in particular fatty fish, on respiratory function and COPD symptoms, mainly among smokers, but none of the studies adjusted for other dietary intakes [111–113]. Contrarily, in a 25-year prospective study conducted in the Netherlands, the intake of n-6 PUFA was positively related to the incidence of chronic lung diseases (defined as chronic productive cough, chronic bronchitis, emphysema, and asthma), but no relation between n-3 PUFA intake and the incidence of chronic nonspecific lung disease was observed [52]. Concordantly, other studies did not find any independent beneficial association between fish intake and FEV1, COPD symptoms [51] or mortality [53]. A large population-based cross-sectional study found that higher intake of individual n-6 PUFAs was associated with lower FEV1 (reduction in FEV1 between the highest vs. lowest quintile of intake = 54.5 mL, 95% CI: –81.6, –27.4, p < 0.0001), particularly in smokers, and with increased risk of COPD, while no association between individual n-3 PUFAs intake and FEV1 or COPD symptoms was seen [114].
More recently, in two large US cohorts, while an initial analysis showed that higher intake of fish (≥4 servings/week), but not PUFAs, was associated with lower risk of newly diagnosed COPD, after adjustment for overall dietary pattern, this association lost significance, suggesting that potential benefits of fish might be evident within the whole diet [115]. Interestingly, fish intake could reduce the risk of COPD when intake of plant sources of n–3 PUFAs is high [115], suggesting that a healthy

diet including fish as well as vegetable sources of n-3 PUFAs may be more beneficial for COPD than isolated food or nutrient.
Evidence exists that anti-inflammatory actions of n-3 PUFA may extend and be relevant to COPD pathogenesis. In an in vitro study, shifting the PUFA supply from AA to DHA significantly reduced the release of pro-inflammatory cytokines (TNF-α, IL-6, and IL-8) and increased the release of anti-inflammatory cytokine (IL-10) from human alveolar cells after endotoxin challenge [116]. Resolvin D1 (derived from DHA) has been reported to inhibit cigarette smoke-induced pro-inflammatory response in human lung cells in vitro and in a mouse model of acute cigarette smoke-induced lung inflammation by selectively activating specific anti-inflammatory pathways, including the inhibition of neutrophilic inflammation and the activation of a subset of anti-inflammatory, pro-resolving macrophages [117]. In stable COPD patients, higher circulating inflammatory markers (IL-6, C-reactive protein) were associated with higher dietary intake of n-6 PUFAs (for IL-6, OR = 1.96, p = 0.034; for CRP, OR = 1.95, p = 0.039), while lower plasma levels of the cytokine TNF-α were related to n-3 PUFAs intake (OR = 0.46, p = 0.049) [118]. Results from feeding trials assessed health outcomes in COPD
patients. An 8-week supplementation with n-3 PUFA (1200 mg ALA, 700 mg EPA, and 340 mg DHA) in patients with moderate-to-severe COPD reversed muscle wasting and improved the functional capacity compared with placebo, without any effect on FEV1 or systemic inflammatory markers (CRP, IL-6, and TNF-α) [119]. Further studies, especially randomized controlled trials, are therefore needed to appraise the relationships between intake of long-chain n-3 PUFA and/or fish and COPD.
6.9. Foods with Potential Deleterious Effects on Lung Function and COPD
Among potential deleterious foods, a statistically significant inverse association between frequent consumption of cured (bacon, hot dogs, and processed meats) and red meats and pulmonary function has been reported, in agreement with evidence of detrimental effects in other nonrespiratory diseases, including CAD, diabetes, and cancer [120,121], and all-cause mortality [122]. Increased intake of cured meats was independently associated with an obstructive pattern of spirometry in a cross-sectional analysis in the third National Health and Nutrition Examination Survey [123] and with an increased risk of newly diagnosed COPD in both men and women in US prospective cohorts, independent of Western dietary pattern (highly loaded with red meat) or other associated dietary intakes (refined grains, desserts, etc.) [124,125]. Importantly, more recent large Swedish population-based prospective studies confirmed this detrimental effect for both baseline and long-term consumption of processed (not unprocessed) red meat [126,127]. Another study found that cured meat intake increased the risk of COPD readmission [128]. Collectively, as summarized in a recent meta-analysis, available evidence indicated a 40% increased risk of COPD with higher consumption of processed red meat (>75–785.5 g/week) [129].
These data suggest that health-promoting activities should include specific advice on lowering red/processed meat consumption. It would be important to confirm these results in those populations experiencing nutrition transition with an increased consumption of Westernized foods, including processed meats.
In addition to the high content in cholesterol and saturated fatty acids, drawbacks of processed red meat include the presence of nitrites, which are added to processed meat during the manufacturing process as a preservative, antimicrobial, and color fixative. Nitrites generate reactive nitrogen species, such as peroxynitrite, with the subsequent nitrosative stress that can contribute to, and amplify, inflammatory processes in the airways and lung parenchyma, causing DNA damage, inhibition of mitochondrial respiration, and cell dysfunction. Moreover, tyrosine nitration in connective tissue proteins, including collagen and elastin, can alter their function. Higher levels of nitrotyrosine have been observed in subjects with COPD and were correlated to disease severity [130]. Accordingly, in animal models, chronic exposure to nitrite caused emphysema-like pathological changes in the lungs [131]. Nitrites are also byproducts of tobacco smoke; thus, nitrite generation may be one of the mechanisms by which tobacco smoke causes COPD. Congruently, the combination of smoking and higher cured

meat consumption is indeed associated with the highest risk of newly diagnosed COPD [125]. Cured meats also contain a high amount of sodium that may increase bronchial hyper-reactivity and may elicit inflammation [132]. Sodium dietary intake has been reported to be higher in COPD patients compared to healthy controls and to be associated with lower lung function [80].
Meat is also an important source of saturated fatty acids (SFAs), which can trigger inflammation, also in the airways [133], and have been associated with both impaired lung function [134] and an elevated risk of coronary heart disease and metabolic diseases [135]. This risk seems to be mainly attributable to medium and long chain SFAs (C14:0–C18:0) highly present in meat compared to other animal sources such as dairy products. By contrast, increased intake of low-fat dairy products [136] as well as of short and medium chain SFAs, as assessed by 24 h recall [137], may exert protective effects on lung function, possibly through their anti-inflammatory action.
An important feature of the Western lifestyle and diet is the consumption of foods with high glycemic index, such as refined grains, desserts, sweets, and sweetened beverages. In addition to increasing the risk of obesity, hyperglycemia may trigger oxidative stress-related inflammatory responses [138], is associated with impaired lung function [139] and poor COPD outcomes [140], and may promote pulmonary infection, at least in part, by an effect on airway glucose concentrations [141]. Part of the detrimental effects of hyperglycemia is mediated by the formation of advanced glycation end-products (AGEs), which are elevated in lung tissues of COPD patients and are known to be associated with lung inflammation and pathophysiology [142]. Compared to no consumption, high levels of soft drink consumption (>0.5 L/day, sweetened or not), an important component of the Western lifestyle and diet, were associated with a higher prevalence of COPD (OR = 1.79, 95% CI: 1.32, 2.43, p < 0.001) and asthma (OR = 1.26, 95% CI: 1.01, 1.58, p = 0.014), in an additive manner with smoking [143]. Moreover, consumption of excess fructose-sweetened soft drink (>5 times/week) was significantly correlated to chronic bronchitis in US adults (OR = 1.80, 95% CI: 1.01, 3.20, p = 0.047) [144], as well as to pediatric asthma [145], possibly due to the formation of AGEs from the interaction between unabsorbed free fructose and dietary proteins in the gastrointestinal tract. These results clearly emphasize the public health implication of interventions targeting modern unhealthy lifestyle habits.

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