Thorkild I A Sørensen

IT University of Copenhagen, København, Capital Region, Denmark

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Publications (557)2898.54 Total impact

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    ABSTRACT: Alcohol consumption, increased body mass index (BMI), and hormone therapy are risk factors for postmenopausal breast cancer, but their combined effects are not well understood. Because hormone therapy is effective for the relief of menopausal symptoms, the identification of "high-risk" users is important for therapeutic reasons. We investigated interactions between hormone therapy use and alcohol-use/high BMI status in relation to invasive breast cancer risk, both overall and according to estrogen receptor (ER) status. Two Danish prospective cohorts were pooled, including 30,789 women aged 50+ years (study period 1981 to 2009). Information on risk factors was obtained in baseline questionnaires. We performed analyses using the Aalen additive hazards model. Serum estradiol and testosterone measurements were obtained in a subsample of approximately 1000 women. During 392,938 person-years of follow-up, 1579 women developed invasive breast cancer. Among nonusers of hormone therapy, the risk of breast cancer was slightly increased with overweight/obesity and increasing alcohol consumption. Compared with normal-weight nonusers, the risk of breast cancer was higher in hormone therapy users across all BMI strata (P for interaction = 0.003). A markedly higher risk of breast cancer was also observed for alcohol combined with hormone therapy use compared with abstinent nonusers (P for interaction = 0.02). These effects were primarily restricted to ER-positive cases. Combined effects of hormone therapy/high BMI and hormone therapy/alcohol on serum estradiol and testosterone supported the hypothesis of a hormonal pathway linking these exposures to breast cancer. These analyses suggest an increased risk of breast cancer associated with hormone therapy use-a risk that may be particularly strong among women consuming alcohol.
    Epidemiology (Cambridge, Mass.) 02/2015; · 6.18 Impact Factor
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    ABSTRACT: Background:Middle-aged obese adults are at substantially elevated risk of oesophageal adenocarcinoma. It is unclear whether this risk originates earlier in life.Methods:We assessed associations between childhood body mass index (BMI) and height-measured annually between ages 7 and 13-with adult oesophageal adenocarcinoma in a cohort from the Copenhagen School Health Records Register. Analyses included 255 053 children born during 1930-1971. Danish Cancer Registry linkage provided outcomes. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression.Results:During 5.4 million person-years of follow-up, 254 (216 males) incident oesophageal adenocarcinomas occurred. At each examined age, cancer risk increased linearly per unit BMI z-score, although associations were only statistically significant for ages 9-13. The HR for the age of 13 years was 1.31 (95% CI: 1.13, 1.51) per unit BMI z-score. Associations were similar in men and women and across birth cohorts. Childhood height was not related to cancer risk in men but was in women, although these analyses included just 38 female cases. HRs per unit height z-score at the age of 13 years were 1.04 (0.90, 1.19) in males and 1.77 (1.27, 2.47) in females, with similar results observed at the other examined ages.Conclusion:Individuals with higher childhood BMI were at elevated risk of oesophageal adenocarcinoma, even though these cancers occurred many decades later in life. Although the mechanisms require further investigation, our findings provide additional evidence for the long-term health risks of childhood obesity.British Journal of Cancer advance online publication, 6 January 2015; doi:10.1038/bjc.2014.646 www.bjcancer.com.
    British Journal of Cancer 01/2015; 112(3). · 4.82 Impact Factor
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    ABSTRACT: Building a population-specific catalogue of single nucleotide variants (SNVs), indels and structural variants (SVs) with frequencies, termed a national pan-genome, is critical for further advancing clinical and public health genetics in large cohorts. Here we report a Danish pan-genome obtained from sequencing 10 trios to high depth (50 × ). We report 536k novel SNVs and 283k novel short indels from mapping approaches and develop a population-wide de novo assembly approach to identify 132k novel indels larger than 10 nucleotides with low false discovery rates. We identify a higher proportion of indels and SVs than previous efforts showing the merits of high coverage and de novo assembly approaches. In addition, we use trio information to identify de novo mutations and use a probabilistic method to provide direct estimates of 1.27e-8 and 1.5e-9 per nucleotide per generation for SNVs and indels, respectively.
    Nature Communications 01/2015; 6:5969. · 10.74 Impact Factor
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    ABSTRACT: We previously used a single nucleotide polymorphism (SNP) in the CHRNA5-A3-B4 gene cluster associated with heaviness of smoking within smokers to confirm the causal effect of smoking in reducing body mass index (BMI) in a Mendelian randomisation analysis. While seeking to extend these findings in a larger sample we found that this SNP is associated with 0.74% lower body mass index (BMI) per minor allele in current smokers (95% CI -0.97 to -0.51, P = 2.00×10-10), but also unexpectedly found that it was associated with 0.35% higher BMI in never smokers (95% CI +0.18 to +0.52, P = 6.38×10-5). An interaction test confirmed that these estimates differed from each other (P = 4.95×10-13). This difference in effects suggests the variant influences BMI both via pathways unrelated to smoking, and via the weight-reducing effects of smoking. It would therefore be essentially undetectable in an unstratified genome-wide association study of BMI, given the opposite association with BMI in never and current smokers. This demonstrates that novel associations may be obscured by hidden population sub-structure. Stratification on well-characterized environmental factors known to impact on health outcomes may therefore reveal novel genetic associations.
    PLoS Genetics 12/2014; · 8.52 Impact Factor
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    ABSTRACT: Animal and human studies suggest that programing of the hypothalamic-pituitary-adrenal (HPA) axis may be involved in the development of obesity, but human studies of biological indicators of HPA axis activity are lacking. We studied the association between levels of the stress hormone cortisol during pregnancy and overweight offspring during childhood into adolescence. Salivary samples from 655 Danish pregnant women with singleton pregnancies (1989-1991) were collected once in the morning and once in the evening in their second and third trimester. We followed the offspring from two to 16 years of age with at least one measurement of height and weight, and classified their body mass index into overweight and normal weight. The adjusted relative difference in median salivary cortisol (with 95% confidence interval (CI)) during pregnancy (the four samples), in second and third trimester (morning and evening samples) between overweight and normal weight offspring was estimated. Furthermore, the adjusted median ratio between morning and evening maternal salivary cortisol level was estimated for normal weight and overweight children. All the analyses were stratified into the equal age groups: 2-6, 7-11, and 12-16 years. We found non-significant higher maternal cortisol levels during pregnancy in offspring that were overweight at the age of 2-6, 7-11 and 12-16 years than in normal weight peers; adjusted relative difference in median salivary cortisol 11% (95% CI: -2; 25), 6% (95% CI: -7; 20), and 9% (95% CI: -4; 24), respectively. A statistically significantly higher level of maternal cortisol was found in the second trimester in 2-6-year-old and 12-16-year-old overweight offspring; relative difference 19% (95% CI: 3; 37), and 20% (95% CI: 3; 41), respectively. The median ratio between morning and evening maternal salivary cortisol level was similar for overweight and normal weight children; e.g. at age 2-6 years in third trimester 4.31 (95% CI: 4.05; 4.60)nmol/l and 4.28 (95% CI: 3.60; 5.09)nmol/l, respectively (P=0.93). Our findings suggest a relatively consistent association between pregnancy cortisol levels and overweight offspring, especially in the second trimester. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Psychoneuroendocrinology 11/2014; 52. · 5.59 Impact Factor
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    ABSTRACT: Energy intake (EI) and physical activity energy expenditure (PAEE) are key modifiable determinants of energy balance, traditionally assessed by self-report despite its repeated demonstration of considerable inaccuracies. We argue here that it is time to move from the common view that self-reports of EI and PAEE are imperfect, but nevertheless deserving of use, to a view commensurate with the evidence that self-reports of EI and PAEE are so poor that they are wholly unacceptable for scientific research on EI and PAEE. While new strategies for objectively determining energy balance are in their infancy, it is unacceptable to use decidedly inaccurate instruments, which may misguide health care policies, future research, and clinical judgment. The scientific and medical communities should discontinue reliance on self-reported EI and PAEE. Researchers and sponsors should develop objective measures of energy balance.International Journal of Obesity accepted article preview online, 13 November 2014. doi:10.1038/ijo.2014.199.
    International journal of obesity (2005) 11/2014; · 5.22 Impact Factor
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    ABSTRACT: We examined mean effects and variance moderating effects of measures of physical activity and fitness on six measures of adiposity and their reciprocal effects in a subsample of the population-representative Danish Twin Registry. Consistent with prior studies, higher levels of physical activity suppressed variance in adiposity, but this study provided further insight. Variance suppression appeared to have both genetic and environmental pathways. Some mean effects appeared due to reciprocal influences of environmental circumstances differing among families but not between co-twins, suggesting these reciprocal effects are uniform. Some variance moderating effects also appeared due to biases in individual measures of adiposity, as well as to differences and inaccuracies in measures of physical activity. This suggests a need to avoid reliance on single measures of both physical activity and adiposity in attempting to understand the pathways involved in their linkages, and constraint in interpreting results if only single measures are available. Future research indications include identifying which physical activity-related environmental circumstances have relatively uniform effects on adiposity in everyone, and which should be individually tailored to maximize motivation to continue involvement.
    Behavior Genetics 10/2014; 45(1). · 2.84 Impact Factor
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    ABSTRACT: Genetic predisposition to adiposity may interact with dietary protein in relation to changes of anthropometry.
    PLoS ONE 10/2014; 9(10):e110890. · 3.53 Impact Factor
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    ABSTRACT: The intergenerational resemblance in body mass index may have increased during the development of the obesity epidemic due to changes in environment and/or expression of genetic predisposition.
    PLoS ONE 10/2014; 9(10):e109932. · 3.53 Impact Factor
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    ABSTRACT: To investigate the association between exposure to mothers smoking during prenatal and early postnatal life and risk of overweight at age 7 years, while taking birth weight into account.
    PLoS ONE 10/2014; 9(10):e109184. · 3.53 Impact Factor
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    ABSTRACT: Objectives Maternal body mass index (BMI), birth weight, and preschool BMI may help identify children at high risk of overweight as they are (1) similarly linked to adolescent overweight at different stages of the obesity epidemic, (2) linked to adult obesity and metabolic alterations, and (3) easily obtainable in health examinations in young children. The aim was to develop early childhood prediction models of adolescent overweight, adult overweight, and adult obesity.Methods Prediction models at various ages in the Northern Finland Birth Cohort born in 1966 (NFBC1966) were developed. Internal validation was tested using a bootstrap design, and external validation was tested for the model predicting adolescent overweight using the Northern Finland Birth Cohort born in 1986 (NFBC1986).ResultsA prediction model developed in the NFBC1966 to predict adolescent overweight, applied to the NFBC1986, and aimed at labelling 10% as “at risk” on the basis of anthropometric information collected until 5 years of age showed that half of those at risk in fact did become overweight. This group constituted one-third of all who became overweight.Conclusions Our prediction model identified a subgroup of children at very high risk of becoming overweight, which may be valuable in public health settings dealing with obesity prevention.
    Obesity 10/2014; · 4.39 Impact Factor
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    ABSTRACT: Background/Objectives:Evidence suggests that the child care environment may be more obesogenic than the family home, and previous studies have found that child care use may be associated with obesity in children. Few studies, however, have focused on child care during infancy, which may be an especially vulnerable period. This study examined child care use in infancy and weight status at 12 months of age in a country where paid maternity leave is common and early child care is not as prevalent as in other developed countries.Subjects/Methods:We studied 27821 children born to mothers participating in the Danish National Birth Cohort (DNBC), a longitudinal study of pregnant women enrolled between 1997 and 2002, who were also included in the Childcare Database, a national record of child care use in Denmark. The exposure was days in child care from birth to 12 months. The outcomes were sex-specific body mass index (BMI) z-score and overweight/obesity (BMI ≥85th percentile based on the World Health Organization classification) at 12 months. We conducted multivariable linear and logistic regression analyses examining child care use and weight outcomes.Results:A total of 17721 (63.7%) children attended child care during their first year of life. After adjustment for potential confounders, a 30-day increment of child care was associated with a modestly higher BMI z-score at 12 months (0.03 units; 95% CI: 0.01, 0.05; p=0.003). Similarly, child care use was associated with increased odds of being overweight/obese at 12 months of age (OR 1.05; 95% CI: 1.01, 1.10; p=0.047).Conclusions:Child care in the first year of life was associated with slightly higher weight at 12 months, suggesting that child care settings may be important targets for obesity prevention in infancy.International Journal of Obesity accepted article preview online, 19 September 2014. doi:10.1038/ijo.2014.173.
    International journal of obesity (2005) 09/2014; · 5.22 Impact Factor
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    ABSTRACT: Greater attained height and greater body mass index (BMI; weight (kg)/height (m)(2)) in young adulthood have been associated with glioma risk, but few studies have investigated the association with body size at birth or during childhood, when the brain undergoes rapid cell growth and differentiation. The Copenhagen School Health Records Register includes data on 320,425 Danish schoolchildren born between 1930 and 1989, with height and weight measurements from ages 7-13 years and parentally recorded birth weights. We prospectively evaluated associations between childhood height and BMI, birth weight, and adult glioma risk. During follow-up (1968-2010), 355 men and 253 women aged ≥18 years were diagnosed with glioma. In boys, height at each age between 7 and 13 years was positively associated with glioma risk; hazard ratios per standard-deviation score at ages 7 (approximately 5.1 cm) and 13 (approximately 7.6 cm) years were 1.17 (95% confidence interval (CI): 1.05, 1.30) and 1.21 (95% CI: 1.09, 1.35), respectively. No associations were observed for childhood height in girls or for BMI. Birth weight was positively associated with risk (per 0.5 kg: hazard ratio = 1.13, 95% CI: 1.04, 1.24). These results suggest that exposures associated with higher birth weight and, in boys, greater height during childhood may contribute to the etiology of adult glioma.
    American Journal of Epidemiology 09/2014; · 4.98 Impact Factor
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    ABSTRACT: The present study examined whether exposure to vitamin D from fortified margarine and milk during prenatal life influenced mean birth weight and the risk of high or low birth weight. The study was based on the Danish vitamin D fortification programme, which was a societal intervention with mandatory fortification of margarine during 1961-1985 and voluntary fortification of low-fat milk between 1972 and 1976. The influence of prenatal vitamin D exposure on birth weight was investigated among 51 883 Danish children, by comparing birth weight among individuals born during 2 years before or after the initiation and termination of vitamin D fortification programmes. In total, four sets of analyses were performed. Information on birth weight was available in the Copenhagen School Health Record Register for all school children in Copenhagen. The mean birth weight was lower among the exposed than non-exposed children during all study periods (milk initiation - 20·3 (95 % CI - 39·2, - 1·4) g; milk termination - 25·9 (95 % CI - 46·0, - 5·7) g; margarine termination - 45·7 (95 % CI - 66·6, - 24·8) g), except during the period around the initiation of margarine fortification, where exposed children were heavier than non-exposed children (margarine initiation 27·4 (95 % CI 10·8, 44·0) g). No differences in the odds of high (>4000 g) or low ( < 2500 g) birth weight were observed between the children exposed and non-exposed to vitamin D fortification prenatally. Prenatal exposure to vitamin D from fortified margarine and milk altered birth weight, but the effect was small and inconsistent, reaching the conclusion that vitamin D fortification seems to be clinically irrelevant in relation to fetal growth.
    British Journal Of Nutrition 09/2014; 112(5):785-793. · 3.34 Impact Factor
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    ABSTRACT: Several studies have shown that adherence to the Mediterranean Diet measured by using the Mediterranean diet score (MDS) is associated with lower obesity risk. The newly proposed Nordic Diet could hold similar beneficial effects. Because of the increasing focus on the interaction between diet and genetic predisposition to adiposity, studies should consider both diet and genetics.
    American Journal of Clinical Nutrition 08/2014; · 6.92 Impact Factor
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    Camilla Schmidt Morgen, Thorkild I A Sørensen
    Nature Reviews Endocrinology 07/2014; · 11.03 Impact Factor
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    ABSTRACT: Physiological evidence indicates that high-protein diets reduce caloric intake and increase thermogenic response, which may prevent weight gain and regain after weight loss. Clinical trials have shown such effects, whereas observational cohort studies suggest an association between greater protein intake and weight gain. In both types of studies the results are based on average weight changes, and show considerable diversity in both directions. This study investigates whether the discrepancy in the evidence could be due to recruitment of overweight and obese individuals into clinical trials.
    PLoS ONE 07/2014; 9(7):e101134. · 3.53 Impact Factor
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    ABSTRACT: Background Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. Methods In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that affect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. Findings In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, −0·12 mm Hg, 95% CI −0·20 to −0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97—0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, −0·02 mm Hg, −0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of −0·10 mm Hg in systolic blood pressure (−0·21 to −0·0001; p=0·0498) and a change of −0·08 mm Hg in diastolic blood pressure (−0·15 to −0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96—0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of −0·29 mm Hg in diastolic blood pressure (−0·52 to −0·07; p=0·01), a change of −0·37 mm Hg in systolic blood pressure (−0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87—0·97; p=0·002). Interpretation Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This finding warrants further investigation in an independent, similarly powered study.
    The Lancet Diabetes and Endocrinology. 06/2014;
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    ABSTRACT: Background:Weight and weight gain throughout infancy are related to later obesity, but whether the strength of the associations varies during the infancy period is uncertain.Aims:Our aims were to identify the period of infancy when change in body weight has the strongest association with adult body mass index (BMI) and also the extent to which these associations during infancy are mediated through childhood BMI.Methods:The Copenhagen Perinatal Cohort, in which participants were followed from birth through 42 years of age, provided information on weight at 12 months and BMI at 42 years for 1 633 individuals. Information on weight at birth, 2 weeks, 1, 2, 3, 4 and 6 months was retrieved from health visitors' records and information on BMI at ages 7 and 13 years from school health records. The associations of infant weight and weight gain standard deviation scores (SDS) with adult BMI-SDS were analyzed using multiple linear regression and path analysis.Results:Higher-weight-SDS at all ages from birth to age 12 months were associated with higher-BMI-SDS at 42 years (regression coefficients 0.08-0.12). Infant weight gain-SDS was associated with greater BMI-SDS at 42 years only between birth and 3 months (0.09, 95% confidence intervals 0.04, 0.15) driven by an association between 2 and 3 months (0.12, 95% confidence intervals (CI) 0.04, 0.20). The latter was partly mediated through later BMI in the path analysis. Infant weight gain-SDS between 3 and 12 months was not associated with greater BMI-SDS at 42 years.Conclusion:Faster weight gain during only the first 3 months of infancy was associated with increased adult BMI, although not in a consistent monthly pattern. Adult BMI is more sensitive to high weight gain during early infancy than late infancy, but not specifically to the first month of life.International Journal of Obesity accepted article preview online, 19 June 2014; doi:10.1038/ijo.2014.108.
    International journal of obesity (2005) 06/2014; · 5.22 Impact Factor
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    ABSTRACT: To investigate if dietary protein and degree of adiposity interacts in relation to change in body weight and waist circumference (WC) in the general population.
    Obesity 06/2014; · 4.39 Impact Factor

Publication Stats

16k Citations
2,898.54 Total Impact Points

Institutions

  • 1983–2015
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 1991–2014
    • University of Copenhagen
      • • Faculty of Health and Medical Sciences
      • • Department of Human Nutrition
      • • Section of Biostatistics
      • • Department of Oral Medicine
      • • Department of Hepatology
      • • Department of Psychology
      København, Capital Region, Denmark
  • 1981–2014
    • Frederiksberg Hospital
      Фредериксберг, Capital Region, Denmark
  • 2013
    • Leiden University Medical Centre
      Leyden, South Holland, Netherlands
  • 2009–2013
    • German Institute of Human Nutrition
      • Department of Epidemiology
      Potsdam, Brandenburg, Germany
    • Aarhus University Hospital
      • Department of Clinical Epidemiology
      Århus, Central Jutland, Denmark
    • Danish Institute for Health Services Research
      København, Capital Region, Denmark
  • 2003–2013
    • University of Southern Denmark
      • • Department of Mathematics and Computer Science
      • • Institute of Public Health
      Odense, South Denmark, Denmark
  • 2002–2013
    • Bispebjerg Hospital, Copenhagen University
      • Institute of Preventive Medicine
      København, Capital Region, Denmark
    • St. Luke's Hospital
      Cedar Rapids, Iowa, United States
  • 1992–2013
    • Institut for Sygdomsforebyggelse
      København, Capital Region, Denmark
  • 1988–2013
    • Copenhagen University Hospital
      København, Capital Region, Denmark
  • 2012
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 1985–2012
    • University of Helsinki
      • • Department of Social Research
      • • Department of Dental Public Health
      Helsinki, Province of Southern Finland, Finland
  • 2011
    • Pierre and Marie Curie University - Paris 6
      • Centre de recherche des Cordeliers - UMR_S 872
      Lutetia Parisorum, Île-de-France, France
    • National Institute for Public Health and the Environment (RIVM)
      Utrecht, Utrecht, Netherlands
    • Rigshospitalet
      • Department of Paediatrics
      Copenhagen, Capital Region, Denmark
    • University of Oslo
      Kristiania (historical), Oslo County, Norway
    • The University of Edinburgh
      • Department of Psychology
      Edinburgh, Scotland, United Kingdom
    • Aalborg University Hospital
      • Department of Cardiology
      Aalborg, Region North Jutland, Denmark
  • 2009–2011
    • Aarhus University
      • • Department of Clinical Epidemiology
      • • National Centre for Integrated Register-based Research "CIRRAU"
      Aars, Region North Jutland, Denmark
  • 1984–2011
    • Copenhagen University Hospital Hvidovre
      • • Department of Clinical Biochemistry
      • • Department of Infectious Diseases
      • • Department of Clinical Physiology and Nuclear Medicine
      • • Department of Cardiology
      Hvidovre, Capital Region, Denmark
  • 2010
    • Imperial College London
      • Department of Epidemiology and Biostatistics
      London, ENG, United Kingdom
    • Roskilde Hospital
      Roskilde, Zealand, Denmark
  • 2003–2009
    • Danish Cancer Society
      København, Capital Region, Denmark
  • 1997–2009
    • Steno Diabetes Center
      Gjentofte, Capital Region, Denmark
  • 2008
    • Baylor College of Medicine
      • Department of Pediatrics
      Houston, TX, United States
  • 2007
    • Odense University Hospital
      • Department of Endocrinology - M
      Odense, South Denmark, Denmark
  • 2005–2007
    • Cornell University
      • Department of Nutritional Sciences
      Ithaca, NY, United States
  • 2002–2007
    • Glostrup Hospital
      • • Department of Ophthalmology
      • • Centre for Preventive Medicine
      Copenhagen, Capital Region, Denmark
  • 1983–2007
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark
  • 2006
    • Exiqon
      København, Capital Region, Denmark
  • 1979–2006
    • Herlev Hospital
      Herlev, Capital Region, Denmark
  • 2004
    • Novo Nordisk
      København, Capital Region, Denmark
    • Statens Serum Institut
      København, Capital Region, Denmark
  • 2003–2004
    • National Institute of Public Health
      København, Capital Region, Denmark
  • 2001
    • CUNY Graduate Center
      New York City, New York, United States
    • Copenhagen Fertility Center
      København, Capital Region, Denmark
  • 1998–2000
    • Copenhagen Trial Unit
      København, Capital Region, Denmark
  • 1989–1991
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States