Nutrition and Respiratory Health—Feature Review
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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.
Vitamin D 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 2D 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.
Minerals 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. Obesity, Adipokines and Respiratory Disease 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 [ ].
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What soil series are you standing on? How has the land in your area been used by humans, over the last two centuries? Who lived here prior to white settlement, and what were their primary subsistence techniques? What was the vegetation type in this area prior to white settlement? Where is there wilderness in your bioregion? What is the elevation above sea level where you live? What is the average annual rainfall for your area? What was the total rainfall in your area last year?
What Spring wildflower is consistently among the first to bloom where you live? Name seven common trees in your area. Which ones are native? For the others, how did they get here? Why were they brought? Which indigenous people inhabit ed your region before you?
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Are they still here? What were the primary subsistence techniques of the culture that lived in your area before you? Name five edible wild plants in your region and their season s of availability. Name three medicinal wild plants in your region, and what they can be used for. Name seven mammals common to your area. Which are native and which are new here? From where did they come?
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