In this study population, nonfasting triglyceride levels were associated with risk of ischemic stroke.

Short telomere length is associated with reduced survival after cancer but not with cancer risk. The latter contrasts with findings from recent meta-analyses.

Background-Lipid profiles are usually measured after fasting. We tested the hypotheses that these levels change only minimally in response to normal food intake and that nonfasting levels predict cardiovascular events. Methods and Results-We cross-sectionally studied 33 391 individuals 20 to 95 years of age from the Copenhagen General Population Study. We also studied 9319 individuals 20 to 93 years of age from the Copenhagen City Heart Study, 1166 of whom developed cardiovascular events during 14 years of follow-up. Compared with fasting levels, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol, and albumin levels were reduced up to 3 to 5 hours after the last meal; triglycerides levels were increased up to 6 hours after the last meal; and non-HDL cholesterol level, apolipoprotein A1 level, apolipoprotein B level, ratio of total cholesterol to HDL cholesterol, and ratio of apolipoprotein B to apolipoprotein A1 did not change in response to normal food intake. The maximum changes after normal food and fluid intake from fasting levels were Ϫ0.2 mmol/L for total cholesterol, Ϫ0.2 mmol/L for low-density lipoprotein cholesterol, Ϫ0.1 mmol/L for HDL cholesterol, and 0.3 mmol/L for triglycerides. Highest versus lowest tertile of nonfasting total cholesterol, non-HDL cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, triglycerides, ratio of total cholesterol to HDL cholesterol, and ratio of apolipoprotein B/apolipoprotein A1 and lowest versus highest tertile of nonfasting HDL cholesterol and apolipoprotein A1 predicted 1.7-to 2.4-fold increased risk of cardiovascular events. Conclusions-Lipid profiles at most change minimally in response to normal food intake in individuals in the general population. Furthermore, nonfasting lipid profiles predicted increased risk of cardiovascular events.

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Objective-We tested the hypothesis that short telomere length is associated with increased risk of myocardial infarction, ischemic heart disease, and early death. Methods and Results-We measured leukocyte telomere length in 2 prospective studies of 19 838 Danish general population participants from the Copenhagen City Heart Study and the Copenhagen General Population Study. Participants were followed for up to 19 years for incident myocardial infarction (nϭ929), ischemic heart disease (nϭ2038), and death (nϭ4342). Follow-up was 100% complete. Telomere length decreased linearly with increasing age in women and men in both studies (Pϭ7ϫ10 Ϫ74 to Pϭ3ϫ10 Ϫ125 ). Multifactorially adjusted hazard ratios were 1.10 (95% CI 1.01-1.19) for myocardial infarction, 1.06 (1.00 -1.11) for ischemic heart disease, and 1.09 (1.05-1.13) for early death per 1000 -base pair decrease in telomere length. The multifactorially adjusted hazard ratios for the shortest versus the longest decile of telomere length were 1.49 (1.07-2.07) for myocardial infarction, 1.24 (1.01-1.53) for ischemic heart disease, and 1.25 (1.07-1.46) for early death. Conclusion-Short telomere length is associated with only modestly increased risk of myocardial infarction, ischemic heart disease, and early death. Key Words: acute coronary syndromes Ⅲ ischemic heart disease Ⅲ death Ⅲ myocardial infarction Ⅲ telomere length T elomeres are protective chromosomal caps at the linear ends of chromosomes consisting of a variable number of TTAGGG repeats. 1 Telomeres shorten with each cell cycle in most cells and therefore reflect organism aging at a cellular level. 1,2 Accordingly, telomere length decreases with increasing age 3,4 but also with male sex, smoking, adiposity, oxidative stress, UV irradiation, and low socioeconomic status. 2,3,[5][6][7] It has therefore been a matter of speculation whether short telomere length is associated with increased risk of cardiovascular disease and early death. 5,8 -10 Previous studies of telomere length and human disease have been limited by cumbersome techniques mainly allowing low-throughput measurements. 11 Furthermore, the majority of studies so far have mainly been smaller case-control studies rather than large prospective studies of unselected individuals from the general population. 12 Accordingly, there is a need for large studies of the general population with extended follow-up, with telomere length measured reliably with a high-throughput method to examine the influence of short telomere length on cardiovascular disease and early death.We tested the hypothesis that short telomere length is associated with increased risk of myocardial infarction, ischemic heart disease, and early death. For this reason, we developed a high-throughput real-time polymerase chain reaction assay calibrated to measure absolute telomere length. Subsequently, we measured 19 838 individuals from 2 prospective studies of the Danish general population from the Copenhagen City Heart Study and the Copenhagen General Population Study, followed for u...

Abstract. Langsted A, Freiberg JJ, Tybjaerg-Hansen A, Schnohr P, Jensen GB, Nordestgaard BG (Herlev Hospital, Herlev; University of Copenhagen; Bispebjerg Hospital; and Rigshospitalet, Copenhagen Ø, Denmark). Nonfasting cholesterol and triglycerides and association with risk of myocardial infarction and total mortality: the Copenhagen City Heart Study with 31 years of follow-up. J Intern Med 2011; 270: 65-75.Objectives. We compared the ability of very high levels of nonfasting cholesterol and triglycerides to predict risk of myocardial infarction and total mortality. Participants. Randomly selected population of 7581 women and 6391 men, of whom 768 and 1151 developed myocardial infarction and 4398 and 4416 died, respectively. Participation rate was 72%, and followup was 100% complete. Less than 2% of participants were taking lipid-lowering therapy. , hazard ratios for myocardial infarction ranged from 1.5 (95%CI: 1.2-1.8) for triglycerides of 1.0-1.99 mmol L )1 to 4.2 (95%CI: 2.5-7.2) for triglycerides ‡5 mmol L )1 (p<0.0001). In men, corresponding hazard ratios ranged from 1.2 (95%CI: 1.0-1.5) to 5.3 (95%CI: 3.6-8.0) for cholesterol (P < 0.0001) and from 1.3 (95%CI: 1.0-1.6) to 2.1 (95%CI: 1.5-2.8) for triglycerides (P < 0.0001). Increasing cholesterol levels were not consistently associated with total mortality in women (trend: P = 0.39) or men (P = 0.02). By contrast, compared with women with triglycerides <1 mmol L )1 , multivariate-adjusted hazard ratios for total mortality ranged from 1.1 (95%CI: 1.0-1.2) for triglycerides of 1.0-1.99 mmol L )1 to 2.0 (95%CI: 1.5-2.9) for triglycerides ‡5 mmol L )1 (trend: P < 0.0001); corresponding hazard ratios in men ranged from 1.1 (95%CI: 1.0-1.2) to 1.5 (95%CI: 1.2-1.7) (P < 0.0001). Conclusions.Stepwise increasing levels of nonfasting cholesterol and nonfasting triglycerides were similarly associated with stepwise increasing risk of myocardial infarction, with nonfasting triglycerides being the best predictor in women and nonfasting cholesterol the best predictor in men. Even more surprisingly, only increasing levels of nonfasting triglycerides were associated with total mortality, whereas increasing cholesterol levels were not.

Background 25-hydroxyvitamin D (25(OH)D) may be associated with lung function through modulation of pulmonary protease-antiprotease imbalance, airway inflammation, lung remodelling and oxidative stress. We examined the association of plasma 25(OH)D levels with lung function, lung function decline and risk of chronic obstructive pulmonary disease (COPD). Methods Plasma 25(OH)D was measured in 10 116 participants in the Copenhagen City Heart Study and in 8391 participants in the Copenhagen General Population Study. In the former study, up to three measurements of lung function spanning 20 years allowed analyses of lung function decline. Results In both cohorts, forced vital capacity in % of predicted was 7% lower and forced expiratory volume in 1 s in % of predicted was 7-10% lower for lowest versus highest decile of 25(OH)D ( p trend ≤1×10 −28). In prospective analyses, participants in the lower versus higher 25(OH)D quintiles had a faster decline in forced expiratory volume in 1 s % predicted (p interaction =1×10 −7) and forced vital capacity % predicted ( p interaction =8×10 −8

BACKGROUND:Increased nonfasting remnant cholesterol, like increased LDL cholesterol, is causally associated with increased risk for ischemic heart disease (IHD). We tested the hypothesis that extreme concentrations of nonfasting remnant and LDL cholesterol are equal contributors to the risk of IHD, myocardial infarction (MI), and all-cause mortality.