SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Hveem Kristian) "

Sökning: WFRF:(Hveem Kristian)

Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Hallan, Andreas, et al. (författare)
  • Risk factors on the development of new-onset gastroesophageal reflux symptoms. A population-based prospective cohort study: the HUNT study
  • 2015
  • Ingår i: American Journal of Gastroenterology. - Stockholm : Karolinska Institutet, Dept of Molecular Medicine and Surgery. - 0002-9270. ; 400
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: Gastroesophageal reflux disease (GERD) is a highly prevalent disorder. This study assessed the risk factors of new-onset gastroesophageal reflux symptoms (GERS). METHODS: The study was based on the HUNT study, a prospective population-based cohort study conducted in 1995-1997 and 2006-2009 in Nord-Trondelag County, Norway. All inhabitants from 20 years of age were invited. Risk factors of new-onset heartburn or acid regurgitation were examined using logistic regression, providing odds ratios (OR) and 95% confidence intervals (CI). RESULTS: A total of 29,610 individuals were included (61% response rate). Participants reporting no GERS at baseline and severe GERS at follow-up (new-onset GERS; n=510) were compared with participants reporting no complaints at both times (n=14,406). Increasing age (OR 1.01 per year, 95% CI 1.00-1.02) was positively associated, whereas male sex (OR 0.81, 95% CI 0.66-0.98) and higher education (OR 0.69, 95% CI 0.56-0.86) were negatively associated with new-onset GERS. Gain in body mass index (BMI) was dose-dependently associated with new-onset GERS (OR 1.30 per unit increase in BMI, 95% CI 1.25-1.35), irrespective of baseline BMI. Previous and current tobacco smoking were associated with new-onset GERS (OR 1.37, 95% CI 1.07-1.76 and OR 1.29, 95% CI 1.00-1.67, respectively). Tobacco smoking cessation was associated with new-onset GERS among those with gain in BMI upon quitting (OR 2.03, 95% CI 1.31-3.16, with >3.5 BMI units increase). CONCLUSIONS: New-onset GERS were associated with increasing age, female sex, lower education, gain in BMI, and ever tobacco smoking. Tobacco smoking cessation was associated with new-onset GERS among those who gained weight upon quitting.
2.
  • Heid, Iris M., et al. (författare)
  • Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution.
  • 2010
  • Ingår i: Nature genetics. - 1546-1718. ; 42:11, s. 949-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Waist-hip ratio (WHR) is a measure of body fat distribution and a predictor of metabolic consequences independent of overall adiposity. WHR is heritable, but few genetic variants influencing this trait have been identified. We conducted a meta-analysis of 32 genome-wide association studies for WHR adjusted for body mass index (comprising up to 77,167 participants), following up 16 loci in an additional 29 studies (comprising up to 113,636 subjects). We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 x 10(-9) to P = 1.8 x 10(-40)) and the known signal at LYPLAL1. Seven of these loci exhibited marked sexual dimorphism, all with a stronger effect on WHR in women than men (P for sex difference = 1.9 x 10(-3) to P = 1.2 x 10(-13)). These findings provide evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.
  •  
3.
  • Heid, Iris M, et al. (författare)
  • Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution
  • 2010
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 42:11, s. 949-960
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Waist-hip ratio (WHR) is a measure of body fat distribution and a predictor of metabolic consequences independent of overall adiposity. WHR is heritable, but few genetic variants influencing this trait have been identified. We conducted a meta-analysis of 32 genome-wide association studies for WHR adjusted for body mass index (comprising up to 77,167 participants), following up 16 loci in an additional 29 studies (comprising up to 113,636 subjects). We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 × 10⁻⁹ to P = 1.8 × 10⁻⁴⁰) and the known signal at LYPLAL1. Seven of these loci exhibited marked sexual dimorphism, all with a stronger effect on WHR in women than men (P for sex difference = 1.9 × 10⁻³ to P = 1.2 × 10⁻¹³). These findings provide evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.</p>
  •  
4.
  • Helgadottir, Anna, et al. (författare)
  • Genome-wide analysis yields new loci associating with aortic valve stenosis
  • 2018
  • Ingår i: Nature Communications. - Nature Publishing Group. - 2041-1723. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Aortic valve stenosis (AS) is the most common valvular heart disease, and valve replacement is the only definitive treatment. Here we report a large genome-wide association (GWA) study of 2,457 Icelandic AS cases and 349,342 controls with a follow-up in up to 4,850 cases and 451,731 controls of European ancestry. We identify two new AS loci, on chromosome 1p21 near PALMD (rs7543130; odds ratio (OR) = 1.20, P = 1.2 × 10-22) and on chromosome 2q22 in TEX41 (rs1830321; OR = 1.15, P = 1.8 × 10-13). Rs7543130 also associates with bicuspid aortic valve (BAV) (OR = 1.28, P = 6.6 × 10-10) and aortic root diameter (P = 1.30 × 10-8), and rs1830321 associates with BAV (OR = 1.12, P = 5.3 × 10-3) and coronary artery disease (OR = 1.05, P = 9.3 × 10-5). The results implicate both cardiac developmental abnormalities and atherosclerosis-like processes in the pathogenesis of AS. We show that several pathways are shared by CAD and AS. Causal analysis suggests that the shared risk factors of Lp(a) and non-high-density lipoprotein cholesterol contribute substantially to the frequent co-occurence of these diseases.
5.
  • Hertel, Jens K., et al. (författare)
  • FTO, Type 2 Diabetes, and Weight Gain Throughout Adult Life A Meta-Analysis of 41,504 Subjects From the Scandinavian HUNT, MDC, and MPP Studies
  • 2011
  • Ingår i: Diabetes. - American Diabetes Association Inc.. - 1939-327X. ; 60:5, s. 1637-1644
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE-FTO is the most important polygene identified for obesity. We aimed to investigate whether a variant in FTO affects type 2 diabetes risk entirely through its effect on BMI and how FTO) influences BMI across adult life span. RESEARCH DESIGN AND METHODS-Through regression models, we assessed the relationship between the FTO single nucleotide polymorphisms rs9939609, type 2 diabetes, and BMI across life span in subjects from the Norwegian population-based HUNT study using cross-sectional and longitudinal perspectives. For replication and meta-analysis, we used data from the Malmo Diet and Cancer (MDC) and Malmo Preventive Project (MPP) cohorts, comprising a total sample of 41,504 Scandinavians. RESULTS-The meta-analysis revealed a highly significant association for rs9939609 with both type 2 diabetes (OR 1.13; P = 4.5 x 10(-8)) and the risk to develop incident type 2 diabetes (OR 1.16; P = 3.2 x 10(-8)). The associations remained also after correction for BMI and other anthropometric measures. Furthermore, we confirmed the strong effect on BMI (0.28 kg/m(2) per risk allele; P = 2.0 x 10(-26), with no heterogeneity between different age-groups. We found no differences in change of BMI over time according to rs9939609 risk alleles, neither overall (Delta BMI = 0.0 [-0.05, 0.05]) nor in any individual age stratum, indicating no further weight gain attributable to FTO genotype in adults. CONCLUSIONS-We have identified that a variant in FTO alters type 2 diabetes risk partly independent of its observed effect on BMI. The additional weight gain as a result of the FTO risk variant seems to occur before adulthood, and the BMI difference remains stable thereafter. Diabetes 60:1637-1644, 2011
  •  
6.
  •  
7.
  •  
8.
  • Lie, Tina Malene, et al. (författare)
  • Snus and risk of gastroesophageal reflux. A population-based case-control study : : the HUNT study
  • 2017
  • Ingår i: Scandinavian Journal of Gastroenterology. - Stockholm : Karolinska Institutet, Dept of Molecular Medicine and Surgery. ; 198
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Tobacco smoking is a risk factor for gastroesophageal reflux, but whether other tobacco products increase the risk is unclear. The aim of this study was to investigate if snus increases the risk of gastroesophageal reflux symptoms (GERS). Material and Methods: The study was based on the third Nord-Trøndelag health study (HUNT3), a population-based study of all adult residents in Nord-Trøndelag County, Norway, performed in 2006−2009. The association between self-reported severe heartburn/regurgitation and snus use was assessed by logistic regression. Results: Compared to never snus users, daily snus users had a reduced risk of GERS (OR 0.77, 95% CI 0.64−0.93), while previous snus users and those using <2 boxes of snus/month had an increased risk (OR 1.20, 95% CI 1.00−1.46 and 1.41, 95% CI 1.02−1.96, respectively). There was no association between age when starting using snus and GERS. Snus users who started using snus to quit or cut down on cigarette smoking, who started using both snus and cigarettes or cigarettes alone had an increased risk of GERS. Snus users <30 years of age had an increased risk of GERS (OR 1.49, 95% CI 1.02−2.16), while those aged between 50−60 and 60−70 years had a reduced risk (OR 0.67, 95% CI 0.49−0.93 and 0.51, 95% CI 0.28−0.94, respectively). Conclusions: Daily snus users had a reduced risk of GERS. However, previous snus users and subgroups of snus users had an increased risk of GERS indicating reverse causality, such that snus use could increase the risk of GERS.
9.
  • Lin, Yulan, et al. (författare)
  • Metabolic syndrome and esophageal and gastric cancer
  • 2015
  • Ingår i: Cancer Causes and Control. - Stockholm : Karolinska Institutet, Dept of Molecular Medicine and Surgery. - 0957-5243. ; 1834
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The role of the metabolic syndrome in the etiology of esophageal and gastric cancer is unclear. METHODS: This was a large nationwide cohort study based on data from 11 prospective population-based cohorts in Norway with long-term follow-up, the Cohort of Norway (CONOR) and the third Nord-Trondelag Health Study (HUNT3). The metabolic syndrome was assessed by objective anthropometric and metabolic biochemical measures and was defined by the presence of at least three of the following five factors: increased waist circumference, elevated triglycerides, low high-density lipoprotein cholesterol, hypertension and high glucose. Newly diagnosed cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma and gastric adenocarcinoma were identified from the Norwegian Cancer Registry. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard models with adjustment for potential confounders. RESULT: Among 192,903 participants followed up for an average of 10.6 years, 62 developed esophageal adenocarcinoma, 64 had esophageal squamous-cell carcinoma and 373 had gastric adenocarcinoma. The metabolic syndrome was significantly associated with an increased risk of gastric adenocarcinoma (HR 1.44, 95% CI 1.14-1.82), but not associated with esophageal adenocarcinoma (HR 1.32, 95% CI 0.77-2.26) or esophageal squamous-cell carcinoma (HR 1.08, 95% CI 0.64-1.83). Increased waist circumference was associated with an increased HR of esophageal adenocarcinoma (HR 2.48, 95% CI 1.27-4.85). No significant association was found between any single component of the metabolic syndrome and risk of esophageal squamous-cell carcinoma. High waist circumference (HR 1.71, 95% CI 1.05-2.80), hypertension (HR 2.41, 95% CI 1.44-4.03) and non-fasting glucose (HR 1.74, 95% CI 1.18-2.56) were also related to an increased risk of gastric adenocarcinoma in women, but not in men. CONCLUSION: Metabolic syndrome was associated with an increased risk of gastric adenocarcinoma in women. Of the individual components of the metabolic syndrome, high waist circumference was positively associated with risk of esophageal adenocarcinoma. Positive associations were also observed for women between high waist circumference, hypertension, high non-fasting glucose and risk of gastric adenocarcinoma. However, further evidence is warranted due to the limited number of cases and the inability to effectively identify gastric cardia adenocarcinoma.
10.
  • Liu, Jimmy Z, et al. (författare)
  • Dense genotyping of immune-related disease regions identifies nine new risk loci for primary sclerosing cholangitis.
  • 2013
  • Ingår i: Nature genetics. - 1546-1718. ; 45:6, s. 670-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Primary sclerosing cholangitis (PSC) is a severe liver disease of unknown etiology leading to fibrotic destruction of the bile ducts and ultimately to the need for liver transplantation. We compared 3,789 PSC cases of European ancestry to 25,079 population controls across 130,422 SNPs genotyped using the Immunochip. We identified 12 genome-wide significant associations outside the human leukocyte antigen (HLA) complex, 9 of which were new, increasing the number of known PSC risk loci to 16. Despite comorbidity with inflammatory bowel disease (IBD) in 72% of the cases, 6 of the 12 loci showed significantly stronger association with PSC than with IBD, suggesting overlapping yet distinct genetic architectures for these two diseases. We incorporated association statistics from 7 diseases clinically occurring with PSC in the analysis and found suggestive evidence for 33 additional pleiotropic PSC risk loci. Together with network analyses, these findings add to the genetic risk map of PSC and expand on the relationship between PSC and other immune-mediated diseases.
  •  
Skapa referenser, mejla, bekava och länka
Åtkomst
fritt online (35)
Typ av publikation
tidskriftsartikel (112)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (112)
övrigt vetenskapligt (3)
Författare/redaktör
Hveem, Kristian (113)
Laakso, Markku, (57)
Kuusisto, Johanna, (54)
Esko, Tonu (54)
Salomaa, Veikko (53)
Jackson, Anne U. (53)
visa fler...
Collins, Francis S. (53)
Metspalu, Andres (53)
McCarthy, Mark I (52)
Boehnke, Michael (51)
Tuomilehto, Jaakko (51)
Luan, Jian'an (50)
Wareham, Nicholas J (49)
Langenberg, Claudia (48)
Mohlke, Karen L (48)
Bonnycastle, Lori L. (48)
Kathiresan, Sekar (47)
Thorleifsson, Gudmar (46)
Hayward, Caroline (46)
Boerwinkle, Eric (46)
Loos, Ruth J. F. (46)
Stringham, Heather M ... (43)
Wilson, James F. (43)
Palmer, Colin N. A. (43)
Rudan, Igor (42)
Lindgren, Cecilia M. (42)
Ferreira, Teresa (41)
Thorsteinsdottir, Un ... (41)
Kanoni, Stavroula (41)
Lakka, Timo A. (41)
Lind, Lars, (40)
Chasman, Daniel I., (40)
Gieger, Christian (40)
Willer, Cristen J. (40)
Perola, Markus (40)
Campbell, Harry (40)
Hofman, Albert (39)
Morris, Andrew P. (39)
Illig, Thomas (39)
Abecasis, Goncalo R. (39)
Stefansson, Kari (39)
Morris, Andrew D (39)
Rauramaa, Rainer (39)
Steinthorsdottir, Va ... (38)
Deloukas, Panos (37)
Stancáková, Alena, (37)
Hamsten, Anders (37)
Ingelsson, Erik (37)
Peters, Annette (37)
Chines, Peter S. (37)
visa färre...
Lärosäte
Karolinska Institutet (37)
Lunds universitet (35)
Umeå universitet (30)
Uppsala universitet (27)
Göteborgs universitet (16)
Högskolan Kristianstad (1)
visa fler...
Stockholms universitet (1)
visa färre...
Språk
Engelska (113)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (109)
Naturvetenskap (3)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy