Top 10: Gasp-worthy Facts about the Respiratory System


Nutrition and the respiratory system.
Dietary antioxidants may have beneficial effects on respiratory health, from influences of the maternal diet on the fetus, and intake in children through to adults and pregnant women with asthma and adults with COPD. Lycopene-rich treatments modify noneosinophilic airway inflammation in asthma: Diet as a risk factor for atopy and asthma. Pharmacological management remains the mainstay for treatment of respiratory diseases, and while treatment options are advancing, dietary intake modification could be an important adjuvant to disease management and an important consideration for disease prevention. A case control study.

Nutritional Requirements of the Respiratory System - KORE Fit Living

Nutrition and Respiratory Health—Feature Review

In COPD, serum levels of vitamin E have been shown to be decreased during exacerbation, which suggests increased intake may be helpful to improve vitamin E concentrations [ 84 ]. The offspring also showed reduced development of lung dendritic cells, necessary for producing allergic responses. Evidence from observational studies also suggests that reduced maternal dietary intake of vitamin E is related to an increased risk of childhood asthma and wheeze [ 90 , 91 , 92 ] and increased in vitro proliferative responses in cord blood mononuclear cells CBMC [ 93 ].

A mechanistic study by Wassall et al. This study by Wassall et al. In asthma the experimental data for vitamin E are compelling, yet supplementation benefits are not well described. Flavonoids are potent antioxidants and have anti-inflammatory as well as anti-allergic actions due in part, to their ability to neutralise ROS [ 95 ]. There are 6 classes of flavonoids including flavones, flavonols, flavanones, isoflavones and flavanols [ 96 ], which are widely distributed throughout the diet and found in fruit, vegetables, nuts, seeds, stems, flowers, roots, bark, dark chocolate, tea, wine and coffee [ 96 ].

Experimental studies of flavonoids in animal models of allergic asthma have shown reduced airway and peripheral blood inflammation, decreased bronchoconstriction and AHR and lower eosinophils in BALF, blood and lung tissue [ , , , ].

In humans, evidence from a case control study in adults showed that apple and red wine consumption, rich sources of flavonoids, was associated with reduced asthma prevalence and severity [ 66 ]. However a follow-up study investigating intake of 3 subclasses of flavonoids did not find any associations with asthma prevalence or severity [ ]. There are a limited number of experimental studies using flavonoid supplements in humans with asthma. There is a paucity of evidence for the effects of flavonoids in the maternal diet and respiratory outcomes in children.

One study which found a positive association of maternal apple intake and asthma in children at 5 years, suggests that the flavonoid content of apples may be responsible for the beneficial relationship [ ].

Evidence for the effects of flavonoids in respiratory conditions is emerging and promising. Though like vitamin C, it may be difficult to disentangle the effects of flavonoids from other nutrients in flavonoid-rich foods. Supplementation of individual flavonoids in experimental animal studies has provided evidence to suggest that intervention trials in humans may be warranted.

Epidemiological studies show promising associations between vitamin D and lung health; however the mechanisms responsible for these effects are poorly understood. Vitamin D can be obtained from dietary sources or supplementation; however sun exposure is the main contributor to vitamin D levels [ ].

While vitamin D has beneficial effects independent of UV exposure [ ], it can be difficult to separate this potential confounder from direct effects of vitamin D on lung health [ ].

The review by Foong and Zosky [ ] presents the current evidence for the role of vitamin D deficiency in disease onset, progression and exacerbation in respiratory infections, asthma and COPD. Respiratory infections contribute to disease progression and exacerbation in both COPD and asthma. Vitamin D appears to have a protective role against the susceptibility to and severity of these infections [ ], as active vitamin D 1,25 OH 2 D modifies production of antimicrobial cathelicidins and defensins that kill bacteria and induce wound repair [ ].

In vitro studies also support the link between vitamin D and airway remodelling as active vitamin D inhibits airway smooth muscle ASM cell proliferation [ ] and deficiency impairs normal lung development [ ]. Furthermore, animal models suggest that vitamin D can inhibit Th1 and Th2 cell cytokine production [ ]. Epidemiological evidence links low levels of vitamin D with wheeze and respiratory infections, though evidence for the link with asthma onset is weak and inconsistent [ ].

In children, low circulating vitamin D was related to lower lung function, increased corticosteroid use and exacerbation frequency [ ]. Also in children with steroid resistant asthma, low vitamin D was related to increased ASM thickness [ ]. Other observational studies report that in children, low levels of vitamin D are associated with asthma exacerbation [ ].

Several observational studies support the role of vitamin D for protection against respiratory conditions in children. The role for vitamin D in enhancing steroid responsiveness suggested by observational studies [ ] is supported by mechanistic studies [ ], and in concert with the actions of vitamin D in infection, may explain the effect of vitamin D in reducing asthma exacerbations [ ].

Only one intervention trial has been conducted using vitamin D in adults with asthma, which found that rate of first exacerbation was reduced in subjects who demonstrated an increase in circulating vitamin D3 following supplementation [ ].

Data for the role of vitamin D in COPD onset is limited, though several cross-sectional studies have reported an association between low vitamin D levels, or deficiency, with COPD incidence [ ].

Experimental data suggest that vitamin D may be important in COPD for its effect on normal lung growth and development, though human data to support this is not available.

It is possible that COPD onset may also be impacted by cellular responses to cigarette smoke exposure which inhibits the protective immunomodulatory effects of vitamin D [ ]. COPD progression may also be affected by vitamin D status through absence of the vitamin D receptor and parenchyma degradation [ ].

COPD exacerbations are generally caused by viral or bacterial lung infections, and though vitamin D has a positive role in reducing infection, there is no evidence to support that vitamin D is associated with ameliorating exacerbations in COPD patients [ ]. The extra-skeletal effects of vitamin D are well documented in both asthma and COPD, and deficiency is associated with negative respiratory and immune outcomes.

Some minerals have also been found to be protective in respiratory conditions. In children, increased intake of magnesium, calcium and potassium is inversely related to asthma prevalence [ 7 ]. While several observational and experimental trials have been performed with conflicting results [ ], a randomised controlled trial concluded that a low sodium diet had no therapeutic benefit for bronchial reactivity in adults with asthma [ ].

Dietary magnesium may have beneficial bronchodilator effects in asthma [ ]. Low dietary magnesium intake has been associated with negative effects on bronchial smooth muscle in severe asthma [ ] and with lower lung function in children [ ].

However further evidence of positive therapeutic effects are required before its importance in asthma and recommendations can be determined [ ]. Dietary intake of selenium has been shown to be lower in asthmatics compared to non-asthmatics [ ] and maternal plasma selenium levels were reported to be inversely associated with risk of asthma in children [ ]. However case control studies in children have not found a relationship with selenium levels or intake with asthma related outcomes [ 18 , ].

Furthermore, results from a large well designed RCT in adults with asthma showed no positive benefit of selenium supplementation [ ]. Investigation of minerals in cord blood imply the importance of adequate intake during pregnancy, as levels of cord blood selenium were negatively associated with persistent wheeze, and levels of iron were negatively associated with later onset wheeze in children [ ].

Studies on dietary intake of minerals and associations with COPD are sparse. A small study in Sweden found that in older subjects with severe COPD, intakes of folic acid and selenium were below recommended levels, and although intake of calcium was adequate, serum calcium levels were low, likely related to their vitamin D status as intake was lower than recommended [ ].

Mineral intake may be important in respiratory diseases, yet evidence for supplementation is weak. It is likely that adequate intake of these nutrients in a whole diet approach is sufficient. Overnutrition and resulting obesity are clearly linked with asthma, though the mechanisms involved are still under investigation. The review by Periyalil et al. In the obese state dietary intake of lipids leads to increased circulating free fatty acids [ ], which activate immune responses, such as activation of TLR4, leading to increased inflammation, both systemically and in the airways [ 20 ].

Adipose tissue also secretes adipokines and asthmatic subjects have higher concentrations of circulating leptin than healthy controls [ 14 ] which are further increased in females, though leptin is associated with BMI in both males and females [ ]. Leptin receptors are present in the bronchial and alveolar epithelial cells and leptin has been shown to induce activation of alveolar macrophages [ ] and have indirect effects on neutrophils [ ].

In vitro , leptin also activates alveolar macrophages taken from obese asthmatics, which induces airway inflammation through production of pro-inflammatory cytokines [ ].

However, a causal role for leptin in the obese asthma relationship is yet to be established. Adiponectin, an anti-inflammatory adipokine, has beneficial effects in animal models of asthma [ ], however, positive associations in human studies have only been seen in women [ ].

In obesity, macrophage and mast cell infiltration into adipose tissue is upregulated [ ]. Neutrophils also appear to dominate airway inflammation in the obese asthma phenotype [ ], particularly in females [ ], which may explain why inhaled corticosteroids are less effective in achieving control in obese asthma [ ].

While the mechanisms are yet to be understood, a recent review reports that obesity in pregnancy is associated with higher odds of asthma in children, with increased risk as maternal BMI increases [ ]. COPD is characterised not only by pulmonary deficits but also by chronic systemic inflammation and co-morbidities which may develop in response to the metabolic dysregulation that occurs with excess adipose tissue [ ].

A recent meta-analysis of leptin levels in COPD reported a correlation with body mass index BMI and fat mass percent in stable COPD though absolute levels were not different to healthy controls [ ]. Adiponectin has anti-inflammatory effects and is present in high concentrations in serum of healthy subjects [ ].

Adiponectin exists in several isoforms, which have varied biological effects [ ] and interact with two receptors present in the lungs AdipoR1 and AdipoR2 that have opposing effects on inflammation [ ]. Single nucleotide polymorphisms in the gene encoding adiponectin are associated with cardiovascular disease, obesity and the metabolic syndrome [ ]. The role of adiponectin in COPD however is not well understood. In COPD, serum adiponectin is increased and directly relates to disease severity and lung function decline [ ].

There is an alteration in the oligomerisation of adiponectin in COPD resulting in increased concentrations of the anti-inflammatory higher-molecular weight isoform [ ], and the expression of adiponectin receptors in the lung is also altered in comparison to healthy subjects [ ]. However under certain conditions in cell lines and animal models adiponectin has been shown to have pro-inflammatory effects [ , ]. As both detrimental and protective effects have been seen, the complex modulation of adiponectin isoforms and receptors in COPD requires further exploration.

Obesity, the resulting systemic inflammation and alterations in adipokines have significant negative effects in both asthma and COPD. While work examining the mechanisms of effect is extensive, evidence for interventions to improve the course of disease are limited to weight loss interventions in asthma at this stage.

Though underweight has not been well studied in asthma, an observational study in Japan reported that subjects with asthma who were underweight had poorer asthma control than their normal weight counterparts [ ]. While there is widespread acknowledgement that malnutrition in pregnant women adversely effects of the lung development of the fetus [ ], a recent review reported that the offspring of mothers who were underweight did not have an increased risk of asthma.

Amongst the obstructive lung diseases, undernutrition is most commonly recognised as a feature of COPD. Weight loss, low body weight and muscle wasting are common in COPD patients with advanced disease and are associated with reduced survival time and an increased risk of exacerbation [ ].

The causes of undernutrition in COPD are multifactorial and include reduced energy intake due to decreased appetite, depression, lower physical activity and dyspnoea while eating [ ]. In addition, resting energy expenditure is increased in COPD, likely due to higher energy demands from increased work of breathing [ ]. Also, systemic inflammation which is a hallmark of COPD, may influence energy intake and expenditure [ ]. Cigarette smoke may also have deleterious effects on body composition in addition to the systemic effects of COPD.

Smoking causes muscle fibre atrophy and decreased muscle oxidative capacity shown in cohorts of non-COPD smokers [ , ] and in animal models of chronic smoke exposure [ , ]. The mechanisms underlying muscle wasting in COPD are complex and multifaceted [ ].

Increased protein degradation occurs in the whole body, though it is enhanced in the diaphragm [ ]. Protein synthesis pathways are altered, indeed insulin like growth factor-1 IGF-1 which is essential for muscle synthesis is decreased in cachectic COPD patients [ ] and is lower in COPD patients during acute exacerbation, compared to healthy controls [ ]. Furthermore myostatin induces muscle atrophy by inhibiting proliferation of myoblasts and mRNA expression of myostain is increased in cachectic COPD patients and is related to muscle mass [ ].

Nutritional supplementation therapy in undernourished COPD patients has been shown to induce weight gain, increase fat free mass, increase grip strength and exercise tolerance as well as improve quality of life [ ]. Further studies point out the importance of not only high energy content, but also macronutrient composition of the nutritional supplement and inclusion of low intensity respiratory rehabilitation exercise [ , ].

Other dietary nutrients have been investigated for the benefits in COPD. Creatinine, found in meat and fish, did not have additive effects to rehabilitation, while sulforaphane, found in broccoli and wasabi, and curcumin, the pigment in turmeric, may have beneficial antioxidant properties [ , , ].

Branched chain amino acid supplementation in COPD is associated with positive results including increases in whole body protein synthesis, body weight, fat free mass and arterial blood oxygen levels [ , ]. Undernutrition is not a significant problem in asthma, though is a major debilitating feature of COPD.

There is promising evidence that nutritional supplementation in COPD is important and can help to alleviate some of the adverse effects of the disease, particularly muscle wasting and weight loss. Dietary intake appears to be important in both the development and management of respiratory diseases, shown through epidemiological and cross-sectional studies and supported by mechanistic studies in animal models.

Although more evidence is needed from intervention studies in humans, there is a clear link for some nutrients and dietary patterns. The dietary patterns associated with benefits in respiratory diseases include high fruit and vegetable intake, Mediterranean style diet, fish and omega-3 intake, while fast food intake and westernised dietary patterns have adverse associations.

Figure 1 shows a diagrammatic representation of the relationships of nutrition and obstructive lung diseases. Relationship of Nutrition and Obstructive Lung Diseases: Dietary factors that have been linked to respiratory disease. Though antioxidants are associated with positive effects on inflammation, clinical outcomes and respiratory disease prevention, intervention studies of individual antioxidants do not indicate widespread adoption of supplementation [ ]. Differences in results from individual studies including whole foods such as fruit and vegetables and fish could be influenced by the nutritional profile owing to the region it was grown or produced.

In considering studies using single nutrients it is also important to acknowledge that nutrients in the diet are consumed as whole foods that contain other micronutrients, fibre and compounds with both known and unknown anti and pro-inflammatory potential.

Furthermore investigations of single nutrients should ideally control for other antioxidants and dietary sources of pro-inflammatory nutrients. While this limitation is common, it is a significant challenge to control for dietary intake of other nutrients in clinical trials. A whole foods approach to nutrient supplementation—for example, increasing intake of fruit and vegetables, has the benefit of increasing intake of multiple nutrients, including vitamin C, vitamin E, carotenoids and flavonoids and shows more promise in respiratory diseases in terms of reducing risk of COPD [ 3 ] and incidence of asthma exacerbations [ 25 ].

The evidence for mechanisms of vitamin D in lung development and immune function are yet to be fully established. It appears that vitamin D is important in respiratory diseases and infections, however the temporal role of vitamin D deficiency in disease onset, pathogenesis and exacerbations and whether supplementation is indicated is yet to be clarified.

Overnutrition in respiratory disease is clearly associated with adverse effects, highlighted by detrimental effects induced by immunometabolism. Further understanding of the relationship between mediators of immunometabolism and respiratory diseases and their mechanisms may provide therapeutic options. Undernutrition still poses risk in some respiratory conditions.

Appropriate nutritional supplementation in advanced COPD is indicated, and several nutrients appear to be beneficial in COPD development and exacerbation. The field of nutrition and respiratory disease continues to develop and expand, though further work is required in the form of randomised controlled dietary manipulation studies using whole foods to enable provision of evidence based recommendations for managing respiratory conditions.

Bronwyn Berthon and Lisa Wood contributed to the study concept and design and were both involved in the preparation and completion of the manuscript.

National Center for Biotechnology Information , U. Journal List Nutrients v. Published online Mar 5. Berthon and Lisa G. Received Jan 19; Accepted Feb This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license http: This article has been cited by other articles in PMC.

Abstract Diet and nutrition may be important modifiable risk factors for the development, progression and management of obstructive lung diseases such as asthma and chronic obstructive pulmonary disease COPD. Introduction Diet and nutrition are increasingly becoming recognised as modifiable contributors to chronic disease development and progression.

Dietary Intake and Respiratory Diseases 2. Dietary Patterns Various dietary patterns have been linked to the risk of respiratory disease [ 7 ]. Fruit and Vegetables Fruit and vegetable intake has been investigated for potential benefits in association with respiratory conditions due to their nutrient profile consisting of antioxidants, vitamins, minerals, fibre and phytochemicals.

Omega-3 Fatty Acids and Fish Omega-3 polyunsaturated fatty acids PUFA from marine sources and supplements have been shown to be anti-inflammatory through several cellular mechanisms including their incorporation into cellular membranes and resulting altered synthesis of eicosanoids [ 31 ].

Nutrients and Respiratory Disease 3. Antioxidants and Oxidative Stress Dietary antioxidants are an important dietary factor in protecting against the damaging effects of oxidative stress in the airways, a characteristic of respiratory diseases [ 50 ]. Vitamin C Vitamin C has been enthusiastically investigated for benefits in asthma and links to asthma prevention. Flavonoids Flavonoids are potent antioxidants and have anti-inflammatory as well as anti-allergic actions due in part, to their ability to neutralise ROS [ 95 ].

Vitamin D Epidemiological studies show promising associations between vitamin D and lung health; however the mechanisms responsible for these effects are poorly understood. Minerals Some minerals have also been found to be protective in respiratory conditions. Obesity, Adipokines and Respiratory Disease Overnutrition and resulting obesity are clearly linked with asthma, though the mechanisms involved are still under investigation.

Undernutrition and Respiratory Disease Though underweight has not been well studied in asthma, an observational study in Japan reported that subjects with asthma who were underweight had poorer asthma control than their normal weight counterparts [ ].

Conclusions Dietary intake appears to be important in both the development and management of respiratory diseases, shown through epidemiological and cross-sectional studies and supported by mechanistic studies in animal models.

Open in a separate window. Author Contributions Bronwyn Berthon and Lisa Wood contributed to the study concept and design and were both involved in the preparation and completion of the manuscript. Conflicts of Interest The authors declare no conflicts of interest. Nutrients and foods for the primary prevention of asthma and allergy: Systematic review and meta-analysis.

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Department of Agriculture's My Plate food guide can guide your chooses in developing a healthy diet that can support not just lung health, but overall well-being. Recent reports by the American Thoracic Society concluded that eating fresh fruits and vegetables, especially those rich in vitamin C, not only improved overall health, but also reduced the incidence of lung disease. The American Thoracic Society also reports that apples and tomatoes particularly seemed to reduce the incidence of respiratory illness.

These fruits also have been shown to increase lung function. The respiratory system is responsible for releasing carbon dioxide from your body and ultimately your lungs.

By eating a balanced diet of carbohydrates, fats and proteins, the body is better able to utilize what it needs through digestion and metabolism. When you eat too much of a single nutrient, the body utilizes more energy trying to regain that balance.

According to the American Lung Association, carbohydrates produce more carbon dioxide than protein or fat. Therefore, a diet high in carbohydrates puts more stress on the respiratory system by requiring the lungs to release an abundance of carbon dioxide. Your daily water intake has a profound effect on your respiratory health. Two-thirds of your body is water, so when you deprive your body of this, much needed nutrient, your respiratory and circulatory system suffer as well as your body in general.

Water keeps the cells plump, which allows water and waste to freely move into and out of the cells.

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