Restrictive Lung Disease Linked to Incident Type 2 Diabetes Laurie Barclay, MD June 10, 2010 Restrictive lung function impairment is associated with incident type 2 diabetes and fatal coronary heart disease (CHD), partially because of traditional and metabolic risk factors and inflammation, according to the results of a prospective study reported online June 2 in Diabetes Care. The association between impaired lung function and cardiovascular disease (CVD) morbidity and mortality is well established, although the mechanisms remain unclear, write S. Goya Wannamethee, PhD, from University College Medical School in London, United Kingdom, and colleagues. Reduced lung function is also one of the many clinical features associated with type 2 diabetes mellitus (T2DM). Diabetes has been shown to be associated with impaired pulmonary function in a restrictive pattern and prospective studies have suggested that reduced lung function may be associated with the development of T2DM. The goals of the study were to prospectively evaluate the associations between lung function and the risk for type 2 diabetes and fatal and non-fatal CHD and to test the hypothesis that inflammation may be the mechanism explaining these associations. At general practices in 24 British towns, 4434 men aged 40 to 59 years with no history of cardiovascular disease (CHD or stroke) or diabetes were recruited and were followed up for 20 years. During follow-up, there were 680 major CHD events, of which 276 were fatal, and 256 incident cases of type 2 diabetes. After adjustment for age, potential confounding variables and metabolic risk factors, forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1), but not FEV1/FVC ratio, were significantly and inversely associated with incident events of type 2 diabetes and fatal CHD, but not nonfatal CHD. For the first vs the fourth quartile of FVC and FEV1, the adjusted relative risk for type 2 diabetes was 1.59 (95% confidence interval [CI], 1.07 - 2.56) and 1.74 (95% CI, 1.16 - 2.61), respectively (P = .03 and P = .04 for trend). For fatal CHD, the corresponding relative risks were 1.48 (95% CI, 1.00 - 2.21; P for trend = .002) and 1.81 (95% CI, 1.19 - 2.76; P = .0003 for trend). There was a significant inverse association between lung function and C-reactive protein (CRP) as well as interleukin 6 (IL-6). After further adjustment for these factors, the inverse associations with type 2 diabetes for FVC and FEV1were no longer statistically significant (P = .14 and P = .11 for trend). However, the inverse associations with type 2 diabetes remained significant for fatal CHD (P = .03 and P = .01, respectively). Restrictive rather than obstructive impairment of lung function is associated with incident T2DM (and fatal CHD) with both associations partially explained by traditional and metabolic risk factors and inflammation, the study authors write. Limitations of this study include low generalizability because the study sample consisted almost exclusively of white European men, possible residual confounding, and inability to determine causality. The association between reduced lung function and fatal CHD and T2DM in particular was to some extent associated with inflammatory pathways, the study authors conclude. Further studies are now needed to extend such novel observations. The association between reduced lung function and development of T2DM and fatal CHD events may provide another possible explanation for the increased risk of fatal CHD in individuals with T2DM. The British Regional Heart Study is supported by program and project grants from the British Heart Foundation. Diabetes Care. Published online June 2, 2010. Abstract
Posted on: Sun, 18 Jan 2015 20:10:30 +0000
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