Thorkild I A Sørensen

University of Bristol, Bristol, England, United Kingdom

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Publications (649)3631.66 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: The aim was to estimate the effects of ponderal index at birth and body mass index (BMI) in early adulthood on C-reactive protein (CRP) and interleukin-6 (IL-6) and to quantify the effects through subsequent measures of body size. In a subanalysis, the contributions of maternal BMI to the inflammatory status of offspring were investigated. Methods: The study was based on 2,986 Danish males from the Copenhagen Aging and Midlife Biobank. Path analysis was employed to estimate direct and indirect effects. Results: A 10% higher maternal BMI was associated with 7% higher CRP and 3% higher IL-6 among offspring. A 10% higher ponderal index at birth was associated with 4% lower CRP in late midlife; this effect was only partially mediated by later growth. A 10% higher BMI in early adulthood was associated with 8% higher CRP and 4% higher IL-6 in late midlife. The findings suggest that weight gain in adulthood is associated with low-grade inflammation in late midlife. Conclusions: Ponderal index at birth is associated with CRP in later life independently of adult BMI. The findings additionally suggest that preventing weight gain in early adulthood would be beneficial for inflammatory status in later life.
    No preview · Article · Dec 2015 · Obesity
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    ABSTRACT: Objective To examine how pre-pregnancy body mass index (BMI), parity, and pregnancy-related weight changes were associated with long-term risk of degenerative musculoskeletal conditions (MSCs). Methods From the Danish National Birth Cohort, 79,687 mothers with singleton births were included. Information on height and weight prior to pregnancy and six months postpartum as well as gestational weight gain was obtained from telephone interviews while parity was derived from the Danish Medical Birth Registry. Diagnoses on MSCs including osteoarthritis, disc disorders, low back pain, and soft tissue disorders were obtained from the Danish National Patient Registry. Hazard ratios (HR) were estimated using Cox regression. Results The cumulative incidence of MSCs during a median follow-up of 12.4 years was 19.7%. Risk of MSCs increased with both increasing pre-pregnancy BMI and increasing parity. Compared to normal-weight first time mothers, the highest risk was seen in obese women with >2 childbirths (HR 1.61 [95% confidence interval 1.41-1.83]). Gestational weight gain of 10-15 kg was associated with the lowest risk of MSCs. Compared to women with no change in weight from pre-conception to weight 6 months after childbirth (±1 BMI unit), increasing postpartum weight increased the risk of MSCs in normal-weight and overweight women. Conclusions High pre-pregnancy BMI increased the risk of degenerative MSC. Also, low and high gestational weight gain, higher postpartum weight retention and especially higher parity were associated with an increased risk. Prevention of maternal overweight both before, during, and after pregnancy may reduce the development of degenerative MSCs among mothers. This article is protected by copyright. All rights reserved.
    No preview · Article · Dec 2015 · Arthritis and Rheumatology
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    Anders Boeck Jensen · Teresa Adeltoft Ajslev · Søren Brunak · Thorkild I A Sørensen
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    ABSTRACT: Objectives The hypothesis of the study was that if the gut microbiota is involved in the development of atherosclerotic cardiovascular and cerebrovascular diseases (CVDs), total colectomy may reduce the long-term risk of CVDs. The aim was therefore to investigate the risk of CVD in patients after a total colectomy compared with patients undergoing other types of surgery, which are not expected to alter the gut microbiota or the CVD risk. Setting The Danish National Patient Register including all hospital discharges in Denmark from 1996 to 2014. Participants Patients (n=1530) aged 45 years and above and surviving 1000 days after total colectomy without CVDs were selected and matched with five control patients who were also free of CVD 1000 days after other types of surgery. The five control patients were randomly selected from each of the three surgical groups: orthopaedic surgery, surgery in the gastrointestinal tract leaving it intact and other surgeries not related to the gastrointestinal tract or CVD (n=22 950). Primary and secondary outcome measures The primary outcome was the first occurring CVD event in any of the seven diagnostic domains (hypertensive disorders, acute ischaemic heart diseases, chronic ischaemic heart disease, cardiac arrhythmias, heart failure, cerebrovascular diseases and other arterial diseases) and the secondary outcomes were the first occurring event within each of these domains. Results Estimated by Cox proportional hazard models, the HRs of the composite CVD end point for patients with colectomy compared with the control patients were not significantly reduced (HR=0.94, 95% confidence limits 0.85 to 1.04). Among the seven CVD domains, only the risk of hypertensive disorders was significantly reduced (HR=0.85, 0.73 to 0.98). Conclusions Colectomy did not reduce the general risk of CVD, but reduced the risk of hypertensive disorders, most likely due to salt and water depletion induced by colectomy. These results encourage a reappraisal of the associations between gut microbiota and CVD.
    Preview · Article · Dec 2015 · BMJ Open
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    ABSTRACT: Association studies have identified a number of loci that contribute to an increased body mass index (BMI), the strongest of which is in the first intron of the FTO gene on human chromosome 16q12.2. However, this region is both non-coding and under strong linkage disequilibrium, making it recalcitrant to functional interpretation. Furthermore, the FTO gene is located within a complex cis-regulatory landscape defined by a topologically associated domain that includes the IRXB gene cluster, a trio of developmental regulators. Consequently, at least three genes in this interval have been implicated in the aetiology of obesity. Here, we sequence a 2 Mb region encompassing the FTO, RPGRIP1L and IRXB cluster genes in 284 individuals from a well-characterised study group of Danish men containing extremely overweight young adults and controls. We further replicate our findings both in an expanded male cohort and an independent female study group. Finally, we compare our variant data with a previous study describing IRX3 and FTO interactions in this region. We obtain deep coverage across the entire region, allowing accurate and unequivocal determination of almost every single nucleotide polymorphism and short insertion/deletion. As well as confirming previous findings across the interval, we identify a further novel age-dependent association upstream of IRX5 that imposes a similar burden on BMI to the FTO locus. Our findings are consistent with the hypothesis that chromatin architectures play a role in regulating gene expression levels across topological domains while our targeted sequence approach represents a widely applicable methodology for high-resolution analysis of regional variation across candidate genomic loci.
    Full-text · Article · Dec 2015 · Genome Medicine
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    Full-text · Dataset · Nov 2015
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    ABSTRACT: A large number of genetic loci are associated with adult body mass index. However, the genetics of childhood body mass index are largely unknown. We performed a meta-analysis of genome-wide association studies of childhood body mass index, using sex- and age-adjusted standard deviation scores. We included 35 668 children from 20 studies in the discovery phase and 11 873 children from 13 studies in the replication phase. In total, 15 loci reached genome-wide significance (P-value < 5 × 10−8) in the joint discovery and replication analysis, of which 12 are previously identified loci in or close to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associated with adult body mass index or childhood obesity. We identified three novel loci: rs13253111 near ELP3, rs8092503 near RAB27B and rs13387838 near ADAM23. Per additional risk allele, body mass index increased 0.04 Standard Deviation Score (SDS) [Standard Error (SE) 0.007], 0.05 SDS (SE 0.008) and 0.14 SDS (SE 0.025), for rs13253111, rs8092503 and rs13387838, respectively. A genetic risk score combining all 15 SNPs showed that each additional average risk allele was associated with a 0.073 SDS (SE 0.011, P-value = 3.12 × 10−10) increase in childhood body mass index in a population of 1955 children. This risk score explained 2% of the variance in childhood body mass index. This study highlights the shared genetic background between childhood and adult body mass index and adds three novel loci. These loci likely represent age-related differences in strength of the associations with body mass index.
    Full-text · Article · Nov 2015 · Human Molecular Genetics
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    ABSTRACT: DNA methylation based biomarkers of aging are highly correlated with actual age. Departures of methylation-estimated age from actual age can be used to define epigenetic measures of child development or age acceleration in adults. Very little is known about genetic or environmental determinants of these epigenetic measures of aging. We obtained DNA methylation profiles using Infinium HumanMethylation450 BeadChips across five time points in 1018 mother-child pairs from the Avon Longitudinal Study of Parents and Children. Using the Horvath age estimation method, we calculated epigenetic age for these samples. Age acceleration (AA) was defined as the residuals from regressing epigenetic age on actual age. AA was tested for associations with cross-sectional clinical variables in children. We identified associations between AA and sex, birth weight, birth by caesarean section and several maternal characteristics in pregnancy, namely smoking, weight, BMI, selenium and cholesterol level. Offspring of non-drinkers had higher AA on average but this difference appeared to resolve during childhood. The associations between sex, birth weight and AA found in ARIES were replicated in an independent cohort (GOYA). In children, epigenetic AA measures are associated with several clinically relevant variables, and early life exposures appear to be associated with changes in AA during adolescence. Further research into epigenetic aging, including the use of causal inference methods, is required to better our understanding of aging.
    Full-text · Article · Nov 2015 · Human Molecular Genetics
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    ABSTRACT: Background: -Smoking is an important cardiovascular disease risk factor, but the mechanisms linking smoking to blood pressure are poorly understood. Methods and results: -Data on 141,317 participants (62,666 never, 40,669 former, 37,982 current smokers) from 23 population-based studies were included in observational and Mendelian randomisation (MR) meta-analyses of the associations of smoking status and smoking heaviness with systolic and diastolic blood pressure (SBP, DBP), hypertension, and resting heart rate. For the MR analyses, a genetic variant rs16969968/rs1051730 was used as a proxy for smoking heaviness in current smokers. In observational analyses, current as compared with never smoking was associated with lower SBP, DBP, and lower hypertension risk, but with higher resting heart rate. In observational analyses amongst current smokers, one cigarette/day higher level of smoking heaviness was associated with higher (0.21 beats/minute; 95% CI 0.19; 0.24) resting heart rate, and slightly higher DBP (0.05 mmHg; 95% CI 0.02; 0.08) and SBP (0.08 mmHg; 95% CI 0.03; 0.13). However, in MR analyses amongst current smokers, while each smoking increasing allele of rs16969968/rs1051730 was associated with higher resting heart rate (0.36 beats/minute/allele; 95% CI 0.18; 0.54), there was no strong association with DBP, SBP, or hypertension. This would suggest a 7 beats/minute higher heart rate in those who smoke 20 cigarettes/day. Conclusions: -This MR meta-analysis supports a causal association of smoking heaviness with higher level of resting heart rate, but not with blood pressure. These findings suggest that part of the cardiovascular risk of smoking may operate through increasing resting heart rate.
    Full-text · Article · Nov 2015 · Circulation Cardiovascular Genetics
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    ABSTRACT: Objective To compare reported birth weight (BW) information in school health records with BW from medical birth records, and to investigate if maternal and offspring characteristics were associated with any discrepancies. Design Register-based cohort study. Setting Denmark, 1973–1991. Participants The study was based on BW recorded in the Copenhagen School Health Records Register (CSHRR) and in The Medical Birth Register (MBR). The registers were linked via the Danish personal identification number. Primary and secondary outcome measures Statistical comparisons of BW in the registers were performed using t tests, Pearson's correlation coefficients, Bland-Altman plots and κ coefficients. Odds of BW discrepancies >100 g were examined by logistic regressions. Results The study population included 47 534 children. From 1973 to 1979 when BW was grouped in 500 g intervals in the MBR, mean BW differed significantly between the registers. During 1979–1991 when BW was recorded in 10 and 1 g intervals, mean BW did not significantly differ between the two registers. BW from both registers was highly correlated (0.93–0.97). Odds of a BW discrepancy significantly increased with parity, the child's age at recall and by marital status (children of married women had the highest odds). Conclusions Overall, BW information in school health records agreed very well with BW from medical birth records, suggesting that reports of BWs in school health records in Copenhagen, Denmark generally are valid.
    Full-text · Article · Nov 2015 · BMJ Open
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    ABSTRACT: Whether the prenatal period is critical for the development of adult primary liver cancer (PLC) is sparsely investigated. Recently, attention has been drawn to potential sex-differences in the early origins of adult disease. The association between birth weight and adult PLC, separately in men and women was investigated, using a large cohort of 217,227 children (51% boys), born from 1936 to 1980, from the Copenhagen School Health Records Register, and followed them until 2010 in national registers. Hazard ratios (95% confidence intervals) of PLC (30 years or older) were estimated by Cox regression models stratified by birth cohort. During 5.1 million person-years of follow-up, 185 men and 65 women developed PLC. Sex modified the association between birth weight and adult PLC (p values for interaction=0.0005). Compared with a sex-specific reference group of birth weights between 3.25 and 3.75 kg, men with birth weights between 2.00 and 3.25 kg and 3.75-5.50 kg, had HRs of 1.48 (1.06-2.05) and 0.85 (0.56-1.28), respectively. Among women the corresponding HRs were 1.71 (0.90-3.29) and 3.43 (1.73-6.82). Associations were similar for hepatocellular carcinoma only, across year of birth, and after accounting for diagnoses of alcohol-related disorders, viral hepatitis and biliary cirrhosis. Prenatal exposures influenced the risk of adult PLC, and the effects at the high birth weight levels appeared to be sex-specific. These findings underscore the importance of considering sex-specific mechanisms in the early origins of adult PLC.
    No preview · Article · Oct 2015 · International Journal of Cancer
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    ABSTRACT: Background: Traffic noise can act as a stressor and disturb sleep, and has been associated with cardiovascular disease. Recent studies suggest a possible association to metabolic outcomes and adiposity through biological mechanisms related to physiological stress and sleep disturbance. Objectives: We aimed to investigate the association between long-term residential traffic noise and changes in adiposity. Materials and methods: The study was based on 39,720 middle-aged Danish men and women from a cohort, with information on weight and waist circumference at two points in time. Residential exposure to traffic noise was calculated for all participants' present and historical addresses using the Nordic prediction method. The associations between traffic noise and changes in adiposity measures after a mean follow-up of 5.3 years were analyzed by linear and logistic regression with adjustments for age, sex, socioeconomic position and lifestyle factors in three models with increasing adjustment. Results: In linear models adjusted for sex, age, socioeconomic position and competing noise sources we found road traffic noise to be significantly associated with small gains in both weight and waist circumference. For example, time-weighted mean exposure 5-years preceding follow-up was associated with a yearly weight gain of 15.4g (95% confidence interval (CI): 2.14; 28.7) and a yearly increase in waist circumference of 0.22mm (95% CI: 0.018; 0.43) per 10dB. Similarly, in Poisson regression models we found an 10% increased risk for gaining more than 5kg body weight during follow-up (95% CI: 1.04; 1.15) per 10dB higher 5 years exposure preceding follow-up. Exposure to railway noise above 55dB was associated with weight gain (39.9g/year (95% CI: 10.2; 69.6)), but not with a significant change in waist circumference. We found baseline BMI (p<0.001) and waist circumference (p=0.001) to be significant effect modifiers for the association between road traffic noise and waist circumference, with gain in waist circumference only among the obese (BMI≥30) participants (1.20mm/year (95% CI: 0.68; 1.72)) and participants with a large waist circumference (0.83mm/year (95% CI: 0.42; 1.23)). Conclusion: The findings supports previous studies suggesting that traffic noise may be associated with development of adiposity. However, the potential effects are small and suggest an effect mainly among obese participants.
    No preview · Article · Oct 2015 · Environmental Research
  • L.G. Andersen · J.L. Baker · T.I.A. Sorensen

    No preview · Article · Oct 2015
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    ABSTRACT: Genome-wide association studies (GWAS) have identified more than 100 genetic variants contributing to BMI, a measure of body size, or waist-to-hip ratio (adjusted for BMI, WHRadjBMI), a measure of body shape. Body size and shape change as people grow older and these changes differ substantially between men and women. To systematically screen for age- and/or sex-specific effects of genetic variants on BMI and WHRadjBMI, we performed meta-analyses of 114 studies (up to 320,485 individuals of European descent) with genome-wide chip and/or Metabochip data by the Genetic Investigation of Anthropometric Traits (GIANT) Consortium. Each study tested the association of up to ~2.8M SNPs with BMI and WHRadjBMI in four strata (men 50y, men >50y, women 50y, women >50y) and summary statistics were combined in stratum-specific meta-analyses. We then screened for variants that showed age-specific effects (G x AGE), sex-specific effects (G x SEX) or age-specific effects that differed between men and women (G x AGE x SEX). For BMI, we identified 15 loci (11 previously established for main effects, four novel) that showed signifi- cant (FDR<5%) age-specific effects, of which 11 had larger effects in younger (<50y) than in older adults (!50y). No sex-dependent effects were identified for BMI. For WHRadjBMI, we identified 44 loci (27 previously established for main effects, 17 novel) with sex-specific effects, of which 28 showed larger effects in women than in men, five showed larger effects in men than in women, and 11 showed opposite effects between sexes. No age-dependent effects were identified for WHRadjBMI. This is the first genome-wide interaction meta-analy- sis to report convincing evidence of age-dependent genetic effects on BMI. In addition, we confirm the sex-specificity of genetic effects on WHRadjBMI. These results may provide further insights into the biology that underlies weight change with age or the sexually dimor- phism of body shape.
    Full-text · Article · Oct 2015 · PLoS Genetics

  • No preview · Article · Oct 2015 · Acta Paediatrica
  • E. Zimmermann · M. Gamborg · T. I. A. Sorensen · J. L. Baker

    No preview · Article · Oct 2015 · Acta Paediatrica

  • No preview · Article · Sep 2015
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    ABSTRACT: We carried out a trans-ancestry genome-wide association and replication study of blood pressure phenotypes among up to 320,251 individuals of East Asian, European and South Asian ancestry. We find genetic variants at 12 new loci to be associated with blood pressure (P = 3.9 x 10(-11) to 5.0 x 10(-21)). The sentinel blood pressure SNPs are enriched for association with DNA methylation at multiple nearby CpG sites, suggesting that, at some of the loci identified, DNA methylation may lie on the regulatory pathway linking sequence variation to blood pressure. The sentinel SNPs at the 12 new loci point to genes involved in vascular smooth muscle (IGFBP3, KCNK3, PDE3A and PRDM6) and renal (ARHGAP24, OSR1, SLC22A7 and TBX2) function. The new and known genetic variants predict increased left ventricular mass, circulating levels of NT-proBNP, and cardiovascular and all-cause mortality (P = 0.04 to 8.6 x 10(-6)). Our results provide new evidence for the role of DNA methylation in blood pressure regulation.
    Full-text · Article · Sep 2015 · Nature Genetics
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    ABSTRACT: A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m 2 in childhood and adolescence and up to 0.2 kg/m 2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.
    Full-text · Article · Sep 2015 · Twin Research and Human Genetics
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    ABSTRACT: Traffic noise has been associated with cardiovascular and metabolic disorders. Potential modes of action are through stress and sleep disturbance, which may lead to endocrine dysregulation and overweight. We aimed to investigate the relationship between residential traffic and railway noise and adiposity. In this cross-sectional study of 57,053 middle-aged people height, weight, waist circumference and bioelectrical impedance were measured at enrolment (1993-1997). Body mass index (BMI), body fat mass index (BFMI) and lean body mass index (LBMI) were calculated. Residential exposure to road and railway traffic noise exposure was calculated using the Nordic prediction method. Associations between traffic noise and anthropometric measures at enrolment were analyzed using general linear models and logistic regression adjusted for demographic and lifestyle factors. Linear regression models adjusted for age, sex and socioeconomic factors showed that five year mean road traffic noise exposure preceding enrolment was associated with a 0.35 cm wider waist circumference (95% CI: 0.21, 0.50) and a 0.18 points higher BMI (95% CI: 0.12, 0.23) per 10 dB. Small, significant increases were also found for BFMI and LBMI. All associations followed linear exposure-response relationships. Exposure to railway noise was not linearly associated with adiposity measures. However, exposure above 60 dB was associated with a 0.71 cm wider waist circumference (95% CI: 0.23, 1.19) and a 0.19 point higher BMI (95% CI: 0.0072, 0.37) compared to unexposed (0-20 dB). The present study finds positive associations between residential exposure to road traffic and railway noise and adiposity.
    No preview · Article · Aug 2015 · Environmental Health Perspectives
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    ABSTRACT: To investigate, using a Mendelian randomisation approach, whether heavier smoking is associated with a range of regional adiposity phenotypes, in particular those related to abdominal adiposity. Mendelian randomisation meta-analyses using a genetic variant (rs16969968/rs1051730 in the CHRNA5-CHRNA3-CHRNB4 gene region) as a proxy for smoking heaviness, of the associations of smoking heaviness with a range of adiposity phenotypes. 148 731 current, former and never-smokers of European ancestry aged ≥16 years from 29 studies in the consortium for Causal Analysis Research in Tobacco and Alcohol (CARTA). Waist and hip circumferences, and waist-hip ratio. The data included up to 66 809 never-smokers, 43 009 former smokers and 38 913 current daily cigarette smokers. Among current smokers, for each extra minor allele, the geometric mean was lower for waist circumference by -0.40% (95% CI -0.57% to -0.22%), with effects on hip circumference, waist-hip ratio and body mass index (BMI) being -0.31% (95% CI -0.42% to -0.19), -0.08% (-0.19% to 0.03%) and -0.74% (-0.96% to -0.51%), respectively. In contrast, among never-smokers, these effects were higher by 0.23% (0.09% to 0.36%), 0.17% (0.08% to 0.26%), 0.07% (-0.01% to 0.15%) and 0.35% (0.18% to 0.52%), respectively. When adjusting the three central adiposity measures for BMI, the effects among current smokers changed direction and were higher by 0.14% (0.05% to 0.22%) for waist circumference, 0.02% (-0.05% to 0.08%) for hip circumference and 0.10% (0.02% to 0.19%) for waist-hip ratio, for each extra minor allele. For a given BMI, a gene variant associated with increased cigarette consumption was associated with increased waist circumference. Smoking in an effort to control weight may lead to accumulation of central adiposity. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Full-text · Article · Aug 2015 · BMJ Open

Publication Stats

25k Citations
3,631.66 Total Impact Points

Institutions

  • 2015
    • University of Bristol
      Bristol, England, United Kingdom
  • 2012-2015
    • Frederiksberg Hospital
      Фредериксберг, Capital Region, Denmark
  • 1998-2015
    • Bispebjerg Hospital, Copenhagen University
      • Institute of Preventive Medicine
      København, Capital Region, Denmark
  • 1977-2015
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 2007-2014
    • Odense University Hospital
      • Department of Endocrinology - M
      Odense, South Denmark, Denmark
    • University of Oulu
      Uleoborg, Northern Ostrobothnia, Finland
    • Cornell University
      • Department of Nutritional Sciences
      Ithaca, NY, United States
  • 2013
    • University of Copenhagen
      • Faculty of Health and Medical Sciences
      Copenhagen, Capital Region, Denmark
    • University of Exeter
      Exeter, England, United Kingdom
  • 2005-2013
    • Aarhus University
      Aarhus, Central Jutland, Denmark
  • 2003-2013
    • University of Southern Denmark
      • Institute of Public Health
      Odense, South Denmark, Denmark
  • 1992-2013
    • Institut for Sygdomsforebyggelse
      København, Capital Region, Denmark
  • 1988-2013
    • Copenhagen University Hospital
      København, Capital Region, Denmark
  • 2010
    • Technical University of Denmark
      Lyngby, Capital Region, Denmark
    • Capital Region Medical Center
      Jefferson City, Missouri, United States
  • 1999-2008
    • Steno Diabetes Center
      Gjentofte, Capital Region, Denmark
  • 2003-2004
    • National Institute of Public Health
      København, Capital Region, Denmark
  • 2002-2004
    • Statens Serum Institut
      • Department of Epidemiology Research
      København, Capital Region, Denmark
    • Laval University
      Quebec City, Quebec, Canada
  • 1978-2003
    • Herlev Hospital
      • Department of Pathology
      Herlev, Capital Region, Denmark
  • 1984-2002
    • Copenhagen University Hospital Hvidovre
      • Department of Clinical Physiology and Nuclear Medicine
      Hvidovre, Capital Region, Denmark
  • 2001
    • Copenhagen Fertility Center
      København, Capital Region, Denmark
  • 1997-2001
    • National University (California)
      San Diego, California, United States
  • 1998-2000
    • Copenhagen Trial Unit
      København, Capital Region, Denmark
  • 1989-1991
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1980-1987
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark
    • Copenhagen University Hospital Gentofte
      Hellebæk, Capital Region, Denmark
  • 1985
    • University of Helsinki
      Helsinki, Southern Finland Province, Finland