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Search Results: 1 - 10 of 2084 matches for " Allan Linneberg "
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The effect of sustained, long-term changes in alcohol intake on cardiovascular risk  [PDF]
Ulla Toft, Charlotta Pisinger, Mette Aadahl, Allan Linneberg, Cathrine Lau, Torben J?rgensen
Open Journal of Preventive Medicine (OJPM) , 2012, DOI: 10.4236/ojpm.2012.24063
Abstract: Objective: To investigate whether sustained long-term changes in alcohol intake are predictive of cardiovascular risk. Methods: The study population was a subpopulation of the five-year intervention study, Inter99 study, (1999-2006), Copenhagen, Denmark (n = 2117; 30 - 60 years). Alcohol intake was assessed by questionnaires at baseline, one-, three- and five-year follow-up. The associations between sustained long-term changes in alcohol intake and cardiovascular risk factors (HDL and non-HDL cholesterol, systolic and diastolic blood pressure (BP); the absolute risk of ischemic heart disease (CRS)) at five-year follow-up were explored by linear regression models. The alcohol variables were tested for linear association with the response variable. Results: Sustained increased alcohol intake was significantly associated with increased CRS (β = 0.0028; P = 0.006) and a decreased HDL cholesterol (β = -0.0028; P = 0.005). Among participants with a moderate overall alcohol in-take at baseline increased alcohol intake was significantly associated with an increased plasma triglyceride (β = 0.0069; P = 0.04). No association with triglyceride was found for participants with a high alcohol intake. Change in wine intake was significantly negatively associated with changes in diastolic BP (β = 0.0015; P = 0.02). Conclusions: Sustained increase in the long-term intake of alcohol was a significant risk factor for an increased CRS, increased triglyceride level and decreased HDL cholesterol. Increased wine intake was associated with decreased diastolic BP.
Variations of CHI3L1, Levels of the Encoded Glycoprotein YKL-40 and Prediction of Fatal and Non-fatal Ischemic Stroke
Camilla Noelle Rathcke, Stine Brinkloev Thomsen, Allan Linneberg, Henrik Vestergaard
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043498
Abstract: Background Polymorphisms of CHI3L1 are associated with inter-individual YKL-40 levels and YKL-40 is associated with an increased mortality and is elevated in patients with cardiovascular disease. We investigated the association between single nucleotide polymorphisms (SNPs) of CHI3L1, serum YKL-40 levels and all-cause and cardiovascular mortality and first-time incidence of myocardial infarction, ischemic heart disease (IHD) and stroke. Methodology/Principal Findings 12 SNPs of CHI3L1 were genotyped and serum YKL-40 was measured in 2656 Danes representative of the general population. Median follow-up period was 15 (0–16) years. Admission data and deaths were ascertained from registers from the Danish National Board of Health. Fourth quartile YKL-40 levels were associated with an increased mortality risk of ischemic stroke (HR 2.44 (1.01–5.88), p = 0.041) and so were homozygotes of the minor allele of rs872129 (HR 9.35 (1.25–69.87, p = 0.022)). Both continuous YKL-40 levels and 4th quartile YKL-40 values (>85 ng/ml) were associated with all-cause mortality (HRs 1.22 (95% CI, 1.10–1.35), p<0.0001, and 1.40 (1.15–1.71), p<0.0001), an increased risk of first-time stroke (HR 1.16 (1.01–1.33), p = 0.04, and 1.63 (1.23–2.16), p = 0.001) and a decreased risk of incidence of IHD (HR 0.77 (0.65–0.91), p = 0.002, and 0.61 (0.44–0.85), p = 0.003). Conclusions/Signficance High YKL-40 levels (>85 ng/ml) and rs872129 were associated with an increased mortality risk of ischemic stroke, but high YKL-40 levels were also inverse related with the risk of incidence of IHD. This could be a chance finding but could also elucidate that YKL-40 plays different roles in development of thromboembolisms versus the formation of local thrombosis.
Analysis of heterogeneity and epistasis in physiological mixed populations by combined structural equation modelling and latent class analysis
Mogens Fenger, Allan Linneberg, Thomas Werge, Torben J?rgensen
BMC Genetics , 2008, DOI: 10.1186/1471-2156-9-43
Abstract: In this study on type 2 diabetes mellitus, heterogeneity was resolved in a latent class framework combined with structural equation modelling using phenotypic indicators of distinct physiological processes. We modelled the clinical condition "the metabolic syndrome", which is known to be a heterogeneous and polygenic condition with a clinical endpoint (type 2 diabetes mellitus). In the model presented here, genetic factors were not included and no genetic model is assumed except that genes operate in networks. The impact of stratification of the study population on genetic interaction was demonstrated by analysis of several genes previously associated with the metabolic syndrome and type 2 diabetes mellitus.The analysis revealed the existence of 19 distinct subpopulations with a different propensity to develop diabetes mellitus within a large healthy study population. The allocation of subjects into subpopulations was highly accurate with an entropy measure of nearly 0.9. Although very few gene variants were directly associated with metabolic syndrome in the total study sample, almost one third of all possible epistatic interactions were highly significant. In particular, the number of interactions increased after stratifying the study population, suggesting that interactions are masked in heterogenous populations. In addition, the genetic variance increased by an average of 35-fold when analysed in the subpopulations.The major conclusions from this study are that the likelihood of detecting true association between genetic variants and complex traits increases tremendously when studied in physiological homogenous subpopulations and on inclusion of epistasis in the analysis, whereas epistasis (i.e. genetic networks) is ubiquitous and should be the basis in modelling any biological process.Despite tremendous progress in our understanding of the human genome and the rapidly advancing ability to probe genetic variation, investigation of the human genome has yielded onl
Mechanistic Understanding of the Effect of Obesity on Asthma and Allergy
Anurag Agrawal,Akshay Sood,Allan Linneberg,Balaram Ghosh
Journal of Allergy , 2013, DOI: 10.1155/2013/598904
Abstract:
Insulin and the Lung: Connecting Asthma and Metabolic Syndrome
Suchita Singh,Y. S. Prakash,Allan Linneberg,Anurag Agrawal
Journal of Allergy , 2013, DOI: 10.1155/2013/627384
Abstract: Obesity, metabolic syndrome, and asthma are all rapidly increasing globally. Substantial emerging evidence suggests that these three conditions are epidemiologically and mechanistically linked. Since the link between obesity and asthma appears to extend beyond mechanical pulmonary disadvantage, molecular understanding is necessary. Insulin resistance is a strong, independent risk factor for asthma development, but it is unknown whether a direct effect of insulin on the lung is involved. This review summarizes current knowledge regarding the effect of insulin on cellular components of the lung and highlights the molecular consequences of insulin-related metabolic signaling cascades that could adversely affect lung structure and function. Examples include airway smooth muscle proliferation and contractility and regulatory signaling networks that are associated with asthma. These aspects of insulin signaling provide mechanistic insight into the clinical evidence for the links between obesity, metabolic syndrome, and airway diseases, setting the stage for novel therapeutic avenues targeting these conditions. 1. Introduction It is now well recognized that obesity and asthma are epidemiologically linked [1–4]. Such a relationship is also seen between asthma and other markers of the metabolic syndrome such as insulin resistance and hypertension that cannot be accounted for by increased body mass alone [4–7]. While both obesity and asthma are individually associated with an increased state of inflammation [8], interestingly, in obese asthmatics, there is a dissociation between cellular inflammation and severity of symptoms, especially in women [9, 10]. This discordance would suggest that while obesity-related systemic inflammation can certainly be one mechanism for increased asthma risk, there is a need to examine mechanisms independent of cellular inflammation that may play a role in asthma in the context of conditions such as obesity and metabolic syndrome. A number of cellular signaling and metabolism mechanisms could contribute to increased asthma risk in patients with obesity and/or metabolic syndrome. Considering the fact that altered glucose metabolism occurs in both cases, and hyperinsulinemia with reduced insulin sensitivity is involved, an obvious potential factor affecting the lung is insulin itself, particularly a direct effect on structural cells as well as immune cells in the airway. In a large Danish cohort, it was observed that insulin resistance (IR) was more strongly related to asthma risk than any of the anthropometric parameters [11]. While
The Association between Genetic Variations of CHI3L1, Levels of the Encoded Glycoprotein YKL-40 and the Lipid Profile in a Danish Population
Stine Brinkl?v Thomsen, Camilla Noelle Rathcke, Tea Skaaby, Allan Linneberg, Henrik Vestergaard
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047094
Abstract: Background The inflammatory biomarker YKL-40 seems to play a role in atherosclerosis and is elevated in patients with obesity, cardiovascular disease and type 2 diabetes. Single nucleotide polymorphisms (SNPs) of the YKL-40 encoding gene, CHI3L1, are associated with inter-individual YKL-40 levels. One study has described an association between a promoter polymorphism of CHI3L1 and levels of low density lipoprotein. The objective of this study was to evaluate the influence of YKL-40 on lipid parameters by determining the association between polymorphisms of CHI3L1, serum YKL-40 and levels of the differentiated lipid profile in a Danish general population. Methodology/Principle Findings 12 SNPs of CHI3L1 were genotyped, and serum YKL-40 and parameters of the lipid profile were measured in 2,656 Danes. Lipid profile and genotypes were available in another Danish population (n = 6,784) for replication. Cholesterol and triglyceride levels increased with increasing YKL-40 quartile (both p<0.0001), and YKL-40 correlated with triglyceride levels (β = 0.15, p<0.0001). Low density lipoprotein levels increased slightly from the 1st to the 3rd quartile (p = 0.006). The highest YKL-40 quartile was associated with a greater risk of hypercholesterolemia compared to the lowest YKL-40 quartile (odds ratio 1.36, p = 0.009). Minor homozygosity of rs12123883 was associated with higher triglyceride levels (p = 0.022) and a higher prevalence of low high density lipoprotein (p = 0.012), but these associations could not be confirmed in the replication population. Conclusions/Significance Serum YKL-40 correlates with triglyceride levels in a representative group of the general Danish population. No consistent associations between SNPs of CHI3L1 and lipid levels could be documented.
Separate and Joint Associations of Occupational and Leisure-Time Sitting with Cardio-Metabolic Risk Factors in Working Adults: A Cross-Sectional Study
Madina Saidj, Torben J?rgensen, Rikke K. Jacobsen, Allan Linneberg, Mette Aadahl
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070213
Abstract: Background The workplace is a main setting for prolonged sitting for some occupational groups. Convincing evidence has recently accumulated on the detrimental cardio-metabolic health effects of leisure-time sitting. Yet, much less is known about occupational sitting, and the potential health risk attached compared to leisure-time sitting. Objective To explore the separate and joint associations of occupational and leisure-time sitting with cardio-metabolic risk factors in working adults. Methods All working adults (N = 2544) from the Health2006, a Danish population-based study, were included in this cross-sectional study. Participants reported hours of sitting during work, during leisure-time along with socio-demographic and behavioral characteristics, including physical activity. Cardio-metabolic risk factors (waist circumference, body mass index, body fat percentage, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, insulin, hemoglobin A1c and plasma glucose) were measured. Associations were explored by linear regression for leisure-time, occupational, and overall sitting time. Results Statistically significant (p<.05) detrimental associations of leisure-time sitting were observed with all cardio-metabolic risk factors, except hemoglobin A1c and plasma glucose. Similarly, occupational sitting time was significantly detrimentally associated with HDL cholesterol, triglycerides, and insulin. For categories of sitting time, a joint adverse association of sitting much during both work-time and leisure-time was observed. Conclusion The associations of occupational sitting time with cardio-metabolic risk factors were fewer and weaker compared to leisure-time sitting. Yet, the joint associations of occupational and leisure-time sitting with cardio-metabolic risk factors were higher than the separate. Our findings amplify the need for further focus in this area prior to making assumptions about equivalent health risks across sedentary behaviors. To our knowledge, this is the first study to contrast the deleterious associations of prolonged occupational and leisure-time sitting, both separately and jointly.
The Association of Alcohol and Alcohol Metabolizing Gene Variants with Diabetes and Coronary Heart Disease Risk Factors in a White Population
Lise Lotte N. Husemoen,Torben J?rgensen,Knut Borch-Johnsen,Torben Hansen,Oluf Pedersen,Allan Linneberg
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011735
Abstract: Epidemiological studies have shown a J- or U-shaped relation between alcohol and type 2 diabetes and coronary heart disease (CHD). The underlying mechanisms are not clear. The aim was to examine the association between alcohol intake and diabetes and intermediate CHD risk factors in relation to selected ADH and ALDH gene variants.
Genetic and Environmental Factors Influencing the Placental Growth Factor (PGF) Variation in Two Populations
Rossella Sorice, Daniela Ruggiero, Teresa Nutile, Mario Aversano, Lotte Husemoen, Allan Linneberg, Catherine Bourgain, Anne-Louise Leutenegger, Marina Ciullo
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042537
Abstract: Placental Growth Factor (PGF) is a key molecule in angiogenesis. Several studies have revealed an important role of PGF primarily in pathological conditions (e.g.: ischaemia, tumour formation, cardiovascular diseases and inflammatory processes) suggesting its use as a potential therapeutic agent. However, to date, no information is available regarding the genetics of PGF variability. Furthermore, even though the effect of environmental factors (e.g.: cigarette smoking) on angiogenesis has been explored, no data on the influence of these factors on PGF levels have been reported so far. Here we have first investigated PGF variability in two cohorts focusing on non-genetic risk factors: a study sample from two isolated villages in the Cilento region, South Italy (N = 871) and a replication sample from the general Danish population (N = 1,812). A significant difference in PGF mean levels was found between the two cohorts. However, in both samples, we observed a strong correlation of PGF levels with ageing and sex, men displaying PGF levels significantly higher than women. Interestingly, smoking was also found to influence the trait in the two populations, although differently. We have then focused on genetic risk factors. The association between five single nucleotide polymorphisms (SNPs) located in the PGF gene and the plasma levels of the protein was investigated. Two polymorphisms (rs11850328 and rs2268614) were associated with the PGF plasma levels in the Cilento sample and these associations were strongly replicated in the Danish sample. These results, for the first time, support the hypothesis of the presence of genetic and environmental factors influencing PGF plasma variability.
Genetic Variant SCL2A2 Is Associated with Risk of Cardiovascular Disease – Assessing the Individual and Cumulative Effect of 46 Type 2 Diabetes Related Genetic Variants
Anders Borglykke, Niels Grarup, Thomas Spars?, Allan Linneberg, Mogens Fenger, J?rgen Jeppesen, Torben Hansen, Oluf Pedersen, Torben J?rgensen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0050418
Abstract: Aim To assess the individual and combined effect of 46 type 2 diabetes related risk alleles on incidence of a composite CVD endpoint. Methods Data from the first Danish MONICA study (N = 3523) and the Inter99 study (N = 6049) was used. Using Cox proportional hazard regression the individual effect of each risk allele on incident CVD was analyzed. Risk was presented as hazard ratios (HR) per risk allele. Results During 80,859 person years 1441 incident cases of CVD (fatal and non-fatal) occurred in the MONICA study. In Inter99 942 incident cases were observed during 61,239 person years. In the Danish MONICA study four gene variants were significantly associated with incident CVD independently of known diabetes status at baseline; SLC2A2 rs11920090 (HR 1.147, 95% CI 1.027–1.283 , P = 0.0154), C2CD4A rs7172432 (1.112, 1.027–1.205 , P = 0.0089), GCKR rs780094 (1.094, 1.007–1.188 , P = 0.0335) and C2CD4B rs11071657 (1.092, 1.007–1.183 , P = 0.0323). The genetic score was significantly associated with increased risk of CVD (1.025, 1.010–1.041, P = 0.0016). In Inter99 two gene variants were associated with risk of CVD independently of diabetes; SLC2A2 (HR 1.180, 95% CI 1.038–1.341 P = 0.0116) and FTO (0.909, 0.827–0.998, P = 0.0463). Analysing the two populations together we found SLC2A2 rs11920090 (HR 1.164, 95% CI 1.070–1.267, P = 0.0004) meeting the Bonferroni corrected threshold for significance. GCKR rs780094 (1.076, 1.010–1.146, P = 0.0229), C2CD4B rs11071657 (1.067, 1.003–1.135, P = 0.0385) and NOTCH2 rs10923931 (1.104 (1.001 ; 1.217 , P = 0.0481) were found associated with CVD without meeting the corrected threshold. The genetic score was significantly associated with increased risk of CVD (1.018, 1.006–1.031, P = 0.0043). Conclusions This study showed that out of the 46 genetic variants examined only the minor risk allele of SLC2A2 rs11920090 was significantly (P = 0.0005) associated with a composite endpoint of incident CVD below the threshold for statistical significance corrected for multiple testing. This potential pathway needs further exploration.
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