The purpose of this study was to examine the associations between smoking, physical inactivity, obesity, and asthma severity among US adults. The magnitude of these associations was very strong. For example, those who visited an emergency room in the past year were 60% more likely than those who did not to smoke; those who used an inhaler > or =15 times in the past month (versus those who did not use an inhaler) were 90% more likely to be physically inactive; and those who had asthma symptoms all the time in the past 30 days (versus those with no symptoms) were 80% more likely to be obese.
"While the study by Gupta et al. may provide in vivo evidence that vitamin D levels are associated with ASM remodeling in children with severe asthma, the cross-sectional nature of the study prevents demonstration of a causal association between vitamin D and ASM (Gupta et al. 2011). Furthermore, vitamin D deficiency is associated with physical inactivity (Strine et al. 2007), which in turn is linked to the severity of asthma (Brock et al. 2010). As such, vitamin D may simply be acting as an indirect marker of physical activity levels. "
[Show abstract][Hide abstract] ABSTRACT: Vitamin D deficiency is associated with disease severity in asthma. We tested whether there is a causal association between vitamin D deficiency, airway smooth muscle (ASM) mass, and the development of airway hyperresponsiveness (AHR). A physiologically relevant mouse model of vitamin D deficiency was developed by raising BALB/c mice on vitamin D-deficient or -replete diets. AHR was assessed by measuring lung function responses to increasing doses of inhaled methacholine. Five-micron sections from formalin-fixed lungs were used for ASM measurement and assessment of lung structure using stereological methods. Transforming growth factor (TGF)-β levels were measured in bronchoalveolar lavage fluid (BALF). Lungs were dissected from embryonic day (E) 17.5 vitamin D-deficient and -replete fetal mice for quantification of ASM density and relative gene expression of TGF-β signaling pathway molecules. Eight-week-old adult vitamin D-deficient female mice had significantly increased airway resistance and ASM in the large airways compared with controls. Vitamin D-deficient female mice had a smaller lung volume, volume of parenchyma, and alveolar septa. Both vitamin D-deficient male and female mice had reduced TGF-β levels in BALF. Vitamin D deficiency did not have an effect on ASM density in E17.5 mice, however, expression of TGF-β1 and TGF-β receptor I was downregulated in vitamin D-deficient female fetal mice. Decreased expression of TGF-β1 and TGF-β receptor I during early lung development in vitamin D-deficient mice may contribute to airway remodeling and AHR in vitamin D-deficient adult female mice. This study provides a link between vitamin D deficiency and respiratory symptoms in chronic lung disease.
"For these patients that smoke, they experience worse control over their asthma as compared with non-smokers with asthma . Previously reported questionnaire and telephone surveys of individuals with asthma provide conclusive evidence that current smoking among asthma patients is associated with a failure to obtain suitable levels of asthma control [1-3]. In turn, smoking cessation among asthma patients has led to improved lung function, reduced use of β2-agonists, lower doses of inhaled corticosteroids required, less frequent daytime asthma symptoms and higher asthma-specific quality of life scores . "
[Show abstract][Hide abstract] ABSTRACT: Cigarette smoking has been associated with accelerated decline in lung function, increased health services use and asthma severity in patients with asthma. Previous studies have provided insight into how smoking cessation improves lung function among asthma patients, however, fail to provide measurable asthma symptom-specific outcomes after smoking cessation. The objective of this study was to measure the effect of changing smoking status on asthma symptom control and health services use in adults with asthma.
The study was conducted in eight primary care practices across Ontario, Canada participating in a community-based, participatory, and evidence-based Asthma Care Program. Patients aged 18 to 55 identified with physician-diagnosed mild to moderate asthma were recruited. In addition to receiving clinical asthma care, participants were administered a questionnaire at baseline and 12-month follow-up visits to collect information on demographics, smoking status, asthma symptoms and routine health services use. The effect of changing smoking status on asthma symptom control was compared between smoking groups using Chi-square and Fisher's exact tests where appropriate. Mixed effect models were used to measure the impact of the change in smoking status on asthma symptom and health services use while adjusting for covariates.
This study included 519 patients with asthma; 11% of baseline smokers quit smoking while 4% of baseline non-smokers started smoking by follow-up. Individuals who quit smoking had 80% lower odds of having tightness in the chest (Odds ratio (OR) = 0.21, 95% CI: 0.06, 0.82) and 76% lower odds of night-time symptoms (OR = 0.24, 95% CI: 0.07, 0.85) compared to smokers who continued to smoke. Compared to those who remained non-smokers, those who had not been smoking at baseline but self-reported as current smoker at follow-up had significantly higher odds of chest tightness (OR = 1.36, 95% CI: 1.10, 1.70), night-time symptoms (OR = 1.55, 95% CI: 1.09, 2.20), having an asthma attack in the last six months (OR = 1.43, 95% CI: 1.17, 1.75) and visiting a walk-in clinic for asthma (OR = 4.57, 95% CI: 1.44, 14.49).
This study provides practitioners measurable and clinically important findings that associate smoking cessation with improved asthma control. Health practitioners and asthma programs can use powerful education messages to emphasize the benefits of smoking cessation as a priority to current smokers.
BMC Public Health 04/2012; 12(1):293. DOI:10.1186/1471-2458-12-293 · 2.26 Impact Factor
"Furthermore, the CXCL5
receptor CXCR2 is expressed in cells other than muscle cells, such as
endothelial, pulmonary, or intestinal epithelial cells. In this context, it is
interesting the recently suggested correlation between obesity and asthma . Strikingly, exacerbation of asthma has been also correlated with increased
expression of both CXCL5 and its receptor CXCR2 . "
[Show abstract][Hide abstract] ABSTRACT: We
have recently shown that the CXCL5 chemokine is secreted by adipose tissue
in the obese state. We demonstrated that adipose tissue-derived CXCL5
mediates insulin resistance in muscle. We speculate in this paper that
CXCL5 could also mediate other obesity, and diabetes-derived pathologies,
such as cardiovascular disease, retinopathy, or inflammatory bowel disease.
In this scenario CXCL5 targeted therapy would prevent not only the
development of type II diabetes in obese subjects, but also several other
obesity-related co morbidities. Finally we propose to analyze the CXCL5
gene to find particular polymorphisms that could predict the development of
type II diabetes in obese subjects.
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