Novel relationship of serum cholesterol with asthma and wheeze in the United States
ABSTRACT Cholesterol exerts complex effects on inflammation. There has been little investigation of whether serum cholesterol is associated with asthma, an inflammatory airways disease with great public health impact.
To determine relationships between levels of 3 serum cholesterol measures (total cholesterol [TC], high-density lipoprotein cholesterol [HDL-C], and non-HDL-C) and asthma/wheeze in a sample representative of the US population.
Cross-sectional study of 7005 participants age >or=6 years from the 2005 to 2006 National Health and Nutrition Examination Survey.
Serum TC and non-HDL-C were lower in patients with current asthma than in subjects without current asthma in the overall population (TC, 188.5 vs 192.2 mg/dL; non-HDL-C, 133.9 vs 137.7 mg/dL; P < .05 for both), whereas HDL-C was not different. Adjusted odds ratios (ORs) from multivariate logistic regression per 1-SD increase of TC and non-HDL-C for current asthma were 0.92 (95% CI, 0.86-0.98) and 0.91 (95% CI, 0.85-0.98), respectively. On racial/ethnic stratification, these relationships reflect marked reductions unique to Mexican Americans (MAs; TC, 171.4 vs 189.3 mg/dL; P < .001; OR, 0.62; 95% CI, 0.48-0.80; non-HDL-C, 119.8 vs 137.9 mg/dL; P < .001; OR, 0.62; 95% CI, 0.48-0.79). Among MAs, the adjusted OR for wheeze requiring medical attention was 0.57 (95% CI, 0.43-0.75) for TC and 0.53 (95% CI, 0.33-0.85) for non-HDL-C. Relationships between cholesterol and asthma/wheeze were independent of body mass index and serum C-reactive protein, and similar between atopic and nonatopic participants.
Serum TC and non-HDL-C are inversely related to asthma in the US population, chiefly reflecting a relationship among MAs.
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ABSTRACT: The joint effect of obesity and asthma on hyperlipidemia has never been explored. We aim to examine (1) the association of dyslipidemia and asthma, (2) the interaction effect of asthma and obesity on hyperlipidemia, and (3) whether a gender difference existed in the above relationships. Between 2009 and 2010, 10- to 15-year-old children were recruited from 7 schools and 2 hospitals in Northern Taiwan. The population consisted of 237 asthmatic children and 225 non-asthmatic controls, and was further divided into four groups: non-obese controls, obese controls, non-obese asthmatics, and obese asthmatics. Measurements included anthropometric measures and blood samples for analysis of metabolic factors. The Cook's criteria were used to define childhood metabolic syndrome. General linear models were used to analyze how lipid profiles were associated with obesity and asthma. Total cholesterol and low density lipoprotein cholesterol levels increased progressively in the group order obese asthmatics>non-obese asthmatics>obese controls>non-obese controls. In boys, low density lipoprotein cholesterol levels were significantly higher in obese asthmatics compared to obese non-asthmatics, with a mean difference of 6.2mmol/L in the general linear model. We also discovered a significant interactive effect of obesity and asthma on hyperlipidemia in boys (p for interaction=0.03). Asthma was associated with higher low density lipoprotein cholesterol levels and this association was amplified in overweight and obese subjects. A gender difference was observed in the joint effect of obesity and asthma on hyperlipidemia.01/2013; 7(1):20-5. DOI:10.1016/j.dsx.2013.02.026
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ABSTRACT: Cholesterol promotes Th2 immunity and allergic inflammation in rodents; whether this occurs in humans is unclear. Reports of both direct and inverse associations between serum cholesterol and atopy in different populations suggest that race and/or other demographic variables may modify these relationships. Aims OF THE STUDY: To determine the relationships between levels of three serum cholesterol measures [total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), and non-HDL-C] and atopy in a sample representative of the US population. Cross-sectional study of 6854 participants aged > or =6 years from the 2005-2006 National Health and Nutrition Examination Survey. In the overall population, adjusted odds ratios (AORs) per two-standard deviation increase in TC and non-HDL-C for biochemical atopy (defined as > or =1 allergen-specific IgE to 19 allergens) were 1.17 [95% confidence interval (CI), 1.00-1.38] and 1.19 (95% CI, 1.03-1.39), respectively. Interactions by race were noted for the two relationships (interaction P = 0.004 and P = 0.009, respectively) with non-Hispanic Whites (NHWs) having direct relationships [TC: AOR 1.27 (95% CI, 1.03-1.57); non-HDL-C: AOR 1.27 (95% CI, 1.03-1.56)] and non-Hispanic Blacks (NHBs) inverse relationships [TC: AOR 0.77 (95% CI, 0.62-0.95); non-HDL-C: AOR 0.86 (95% CI, 0.69-1.08)]. The adjusted HDL-C-atopy relationship was nonsignificant for NHWs and inverse for NHBs [AOR 0.77 (95% CI, 0.61-0.96)]. Relationships were independent of body mass index and serum C-reactive protein and unmodified by corticosteroid or statin usage. Results were similar using current hay fever/allergy as the atopy outcome. There are marked inter-racial differences in the relationship between serum cholesterol and atopy in the US population.Allergy 12/2009; 65(7):859-64. DOI:10.1111/j.1398-9995.2009.02287.x · 6.00 Impact Factor
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ABSTRACT: Dyslipidemia influences innate immune responses in the bloodstream, but whether and how pulmonary innate immunity is sensitive to circulating lipoproteins is largely unknown. To define whether dyslipidemia impacts responses to bacteria in the airspace and, if so, whether differently from its effects in other tissues, airspace, bloodstream, and i.p. responses to LPS and Klebsiella pneumoniae were investigated using murine models of dyslipidemia. Dyslipidemia reduced neutrophil (PMN) recruitment to the airspace in response to LPS and K. pneumoniae by impairing both chemokine induction in the airspace and PMN chemotaxis, thereby compromising pulmonary bacterial clearance. Paradoxically, bacteria were cleared more effectively from the bloodstream during dyslipidemia. This enhanced systemic response was due, at least in part, to basal circulating neutrophilia and basal TLR4/MyD88-dependent serum cytokine induction and enhanced serum cytokine responses to systemically administered TLR ligands. Dyslipidemia did not globally impair PMN transvascular trafficking to, and host defense within all loci, because neutrophilia, cytokine induction, and bacterial clearance were enhanced within the infected peritoneum. Peritoneal macrophages from dyslipidemic animals were primed for more robust TLR responses, reflecting increased lipid rafts and increased TLR4 expression, whereas macrophages from the airspace, in which cholesterol was maintained constant during dyslipidemia, had normal responses and rafts. Dyslipidemia thus imparts opposing effects upon intra- and extrapulmonary host defense by inducing tissue-divergent TLR response phenotypes and dysregulating airspace/blood compartmental levels of PMNs and cytokines. We propose that the airspace is a "privileged" site, thereby uniquely sensitive to dyslipidemia.The Journal of Immunology 08/2010; 185(3):1660-9. DOI:10.4049/jimmunol.0903501 · 5.36 Impact Factor