Thorkild I A Sørensen

Frederiksberg Hospital, Фредериксберг, Capital Region, Denmark

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Publications (393)1817.71 Total impact

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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;
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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.
    The British journal of nutrition. 09/2014; 112(5):785-793.
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    Human Molecular Genetics 08/2014; · 7.69 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; · 6.50 Impact Factor
  • Camilla Schmidt Morgen, Thorkild I A Sørensen
    Nature Reviews Endocrinology 07/2014; · 11.03 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; · 3.92 Impact Factor
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    ABSTRACT: The 12th Stock Conference addressed body composition and related functions in two extreme situations, obesity and cancer cachexia. The concept of ‘functional body composition’ integrates body components into regulatory systems relating the mass of organs and tissues to corresponding in vivo functions and metabolic processes. This concept adds to an understanding of organ/tissue mass and function in the context of metabolic adaptations to weight change and disease. During weight gain and loss, there are associated changes in individual body components while the relationships between organ and tissue mass are fixed. Thus an understanding of body weight regulation involves an examination of the relationships between organs and tissues rather than individual organ and tissue masses only. The between organ/tissue mass relationships are associated with and explained by crosstalks between organs and tissues mediated by cytokines, hormones and metabolites that are coupled with changes in body weight, composition and function as observed in obesity and cancer cachexia. In addition to established roles in intermediary metabolism, cell function and inflammation, organ-tissue crosstalk mediators are determinants of body composition and its change with weight gain and loss. The 12th Stock Conference supported Michael Stocks' concept of gaining new insights by integrating research ideas from obesity and cancer cachexia. The conference presentations provide an in-depth understanding of body composition and metabolism.
    Obesity Reviews 06/2014; · 6.87 Impact Factor
  • J Aarestrup, M Gamborg, M B Cook, T I A Sørensen, J L Baker
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    ABSTRACT: Background:Prostate cancer aetiology is poorly understood. It may have origins early in life; previously we found a positive association with childhood height. The effects of early life body mass index (BMI; kg m(-2)) on prostate cancer remain equivocal. We investigated if childhood BMI, independently and adjusted for height, is positively associated with adult prostate cancer.Methods:Subjects were a cohort of 125 208 boys formed from the Copenhagen School Health Records Register, born 1930-1969 with height and weight measurements at 7-13 years. Cases were identified through linkage to the Danish Cancer Registry. Cox proportional hazards regressions were performed.Results:Overall, 3355 men were diagnosed with prostate cancer. Body mass index during childhood was positively associated with adult prostate cancer. The hazard ratio of prostate cancer was 1.06 (95% confidence interval (CI): 1.01-1.10) per BMI z-score at age 7, and 1.05 (95% CI: 1.01-1.10) per BMI z-score at age 13. Estimates were similar and significant at all other ages. However, adjustment for childhood height attenuated the associations at all but the youngest ages as most estimates became nonsignificant.Conclusions:These results suggest that at most childhood ages, BMI does not confer an additional risk for prostate cancer beyond that of height.British Journal of Cancer advance online publication, 27 May 2014; doi:10.1038/bjc.2014.266 www.bjcancer.com.
    British journal of cancer. 05/2014;
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    ABSTRACT: Background:In contrast to the physiological expectation, observational studies show that greater protein intake is associated with subsequent body weight (BW) gain. An increase in fat-free mass (FFM) due to anabolic effects of protein could explain this.Objective:To examine associations between protein intake and subsequent changes in fat mass (FM) and FFM in longitudinal, observational data.Design:A health examination, including measures of FM and FFM by bioelectrical impedance at baseline and follow-up six years later, was conducted. Diet history interviews (DHI) were performed, and 24-hour urinary nitrogen collection at baseline was done. In total, 330 participants with DHI, of whom 227 had validated and complete 24-hour urine collection, were analyzed. Macronutrient energy substitution models were used.Results:Mean estimated protein intake was 14.6 E% from DHI and 11.3 E% from urinary nitrogen. Estimated from DHI, FM increased 46 gram/year with every 1 E% protein substituted for fat (95%CI: 13, 79; P=0.006) and FFM increased 15 gram/year (1, 30; P=0.046). Results were similar in other substitution models. Estimated from urinary nitrogen, FM increased 53 gram/year with 1 E% protein substituted for other macronutrients (24, 81; p<0.0005), and FFM increased 18 gram/year (6, 31; P=0.004).Conclusion:Within a habitual range, a greater protein intake was associated with BW gain, mostly in FM. This is in contrast to the expectations based on physiological and clinical trials, and calls for a better understanding of how habitual dietary protein influences long-term energy balance, versus how greater changes in dietary proteins may influence short-term energy balance.International Journal of Obesity accepted article preview online, 20 May 2014; doi:10.1038/ijo.2014.80.
    International journal of obesity (2005) 05/2014; · 5.22 Impact Factor
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    ABSTRACT: The genetic contribution to the variation in human lifespan is approximately 25%. Despite the large number of identified disease-susceptibility loci, it is not known which loci influence population mortality.We performed a genome-wide association meta-analysis of 7729 long-lived individuals of European descent (≥ 85 years) and 16121 younger controls (< 65 years) followed by replication in an additional set of 13060 long-lived individuals and 61156 controls. In addition, we performed a subset analysis in cases≥90 years.We observed genome-wide significant association with longevity, as reflected by survival to ages beyond 90 years, at a novel locus, rs2149954, on chromosome 5q33.3 (OR=1.10, P =1.74 x 10(-8)). We also confirmed association of rs4420638 on chromosome 19q13.32 (OR=0.72, P=3.40 x 10(-36)), representing the TOMM40/APOE/APOC1 locus. In a prospective meta-analysis (n=34103) the minor allele of rs2149954 (T) on chromosome 5q33.3 associates with increased survival (HR=0.95, P=0.003). This allele has previously been reported to associate with low blood pressure in middle age. Interestingly, the minor allele (T) associates with decreased cardiovascular mortality risk, independent of blood pressure.We report on the first GWAS-identified longevity locus on chromosome 5q33.3 influencing survival in the general European population. The minor allele of this locus associates with low blood pressure in middle age, although the contribution of this allele to survival may be less dependent on blood pressure. Hence, the pleiotropic mechanisms by which this intragenic variation contributes to lifespan regulation have to be elucidated.
    Human Molecular Genetics 03/2014; · 7.69 Impact Factor
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    ABSTRACT: We analysed single nucleotide polymorphisms (SNPs) tagging the genetic variability of six candidate genes (ATF6, FABP1, LPIN2, LPIN3, MLXIPL and MTTP) involved in the regulation of hepatic lipid metabolism, an important regulatory site of energy balance for associations with body mass index (BMI) and changes in weight and waist circumference. We also investigated effect modification by sex and dietary intake. Data of 6,287 individuals participating in the European prospective investigation into cancer and nutrition were included in the analyses. Data on weight and waist circumference were followed up for 6.9 ± 2.5 years. Association of 69 tagSNPs with baseline BMI and annual changes in weight as well as waist circumference were investigated using linear regression analysis. Interactions with sex, GI and intake of carbohydrates, fat as well as saturated, monounsaturated and polyunsaturated fatty acids were examined by including multiplicative SNP-covariate terms into the regression model. Neither baseline BMI nor annual weight or waist circumference changes were significantly associated with variation in the selected genes in the entire study population after correction for multiple testing. One SNP (rs1164) in LPIN2 appeared to be significantly interacting with sex (p = 0.0003) and was associated with greater annual weight gain in men (56.8 ± 23.7 g/year per allele, p = 0.02) than in women (-25.5 ± 19.8 g/year per allele, p = 0.2). With respect to gene-nutrient interaction, we could not detect any significant interactions when accounting for multiple testing. Therefore, out of our six candidate genes, LPIN2 may be considered as a candidate for further studies.
    Genes & Nutrition 03/2014; 9(2):385. · 3.33 Impact Factor
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    ABSTRACT: BACKGROUND: Studies indicate an effect of dietary calcium on change in body weight (BW) and waist circumference (WC), but the results are inconsistent. Furthermore, a relation could depend on genetic predisposition to obesity. OBJECTIVE: The objective was to examine whether genetic predisposition to higher body mass index (BMI), WC, or waist-hip ratio (WHR) interacts with dietary calcium in relation to subsequent annual change in BW (ΔBW) and WC (ΔWC). DESIGN: The study is based on 7569 individuals from the MONItoring trends and determinants of CArdiovascular disease Study, a sample from the Danish Diet, Cancer and Health Study and the INTER99 study, with information on diet; 54 single-nucleotide polymorphisms (SNPs) associated with BMI, WC, or WHR adjusted for BMI; and potential confounders. The SNPs were combined in 4 scores as indicators of genetic predisposition; all SNPs in a general score and a score for each of 3 phenotype: BMI, WC, and WHR. Linear regression was used to examine the association between calcium intake and ΔBW or ΔWC adjusted for concurrent ΔBW. SNP score × calcium interactions were examined by adding product terms to the models. RESULTS: We found a significant ΔBW of -0.076 kg (P = 0.021; 95% CI: -0.140, -0.012) per 1000 mg Ca. No significant association was observed between dietary calcium and ΔWC. In the analyses with ΔBW as outcome, we found no significant interactions between the developed predisposition scores and calcium. However, we found a significant interaction between a score of 6 WC-associated SNPs and calcium in relation to ΔWC. Each risk allele was associated with a ΔWC of -0.043 cm (P = 0.038; 95% CI: -0.083, -0.002) per 1000 mg Ca. CONCLUSIONS: Our study suggests that dietary calcium relates weakly to BW loss. We found no evidence of a general association between calcium and ΔWC, but calcium may reduce WC among people genetically predisposed to a high WC. However, further replication of this finding is needed.
    American Journal of Clinical Nutrition 02/2014; · 6.50 Impact Factor
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    ABSTRACT: An association between maternal pre-pregnancy BMI and childhood intelligence quotient (IQ) has repeatedly been found but it is unknown if this association is causal or due to confounding caused by genetic or social factors. We used a cohort of 1,783 mothers and their 5-year-old children sampled from the Danish National Birth Cohort. The children participated between 2003 and 2008 in a neuropsychological assessment of cognitive ability including IQ tests taken by both the mother and the child. Linear regression analyses were used to estimate the associations between parental BMI and child IQ adjusted for a comprehensive set of potential confounders. Child IQ was assessed with the Wechsler Primary and Preschool Scales of Intelligence - Revised (WPPSI-R). The crude association between maternal BMI and child IQ showed that BMI was adversely associated with child IQ with a reduction in IQ of -0.40 point for each one unit increase in BMI. This association was attenuated after adjustment for social factors and maternal IQ to a value of -0.27 (-0.50 to -0.03). After mutual adjustment for the father's BMI and all other factors except maternal IQ, the association between paternal BMI and child IQ yielded a regression coefficient of -0.26 (-0.59 to 0.07), which was comparable to that seen for maternal BMI (-0.20 (-0.44 to 0.04)). Although maternal pre-pregnancy BMI was inversely associated with the IQ of her child, the similar association with paternal BMI suggests that it is not a specific pregnancy related adiposity effect.
    PLoS ONE 01/2014; 9(4):e94498. · 3.53 Impact Factor
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    Laura D Howe, Esther Zimmermann, Ram Weiss, Thorkild I A Sørensen
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    ABSTRACT: Some obese individuals have no cardiometabolic abnormalities; they are 'metabolically healthy, but obese' (MHO). Similarly, some non-obese individuals have cardiometabolic abnormalities, that is, 'metabolically at risk, normal weight' (MANW). Previous studies have suggested that early-onset obesity may be associated with MHO. We aimed to assess whether body mass index (BMI) in childhood and early-onset obesity are associated with MHO. General population longitudinal cohort study, Denmark. From 362 200 young men (mean age 20) examined for Danish national service between 1943 and 1977, all obese men (BMI ≥31 kg/m(2), N=1930) were identified along with a random 1% sample of the others (N=3601). Our analysis includes 2392 of these men attending a research clinic in mid-life (mean age 42). For 613 of these men, data on childhood BMI are available. We summarised childhood BMI growth (7-13 years) using a multilevel model. Early-onset obesity was defined as obesity at examination for national service. We defined metabolic health at the mid-life clinic as non-fasting serum cholesterol <6.6 mmol/L, non-fasting glucose <8.39 mmol/L and pulse pressure <48 mm Hg. Participants were categorised into four groups according to their obesity (BMI ≥30 kg/m(2)) and metabolic health in mid-life. 297 of 1097 (27.1%) of obese men were metabolically healthy; 826 of 1295 (63.8%) non-obese men had at least one metabolic abnormality. There was no evidence that rapid BMI growth in childhood or early-onset obesity was associated with either MHO or the MANW phenotype, for example, among obese men in mid-life, the OR for MHO comparing early-onset obesity with non-early-onset obesity was 0.97 (95% CI 0.85 to 1.10). We found no robust evidence that early-onset obesity or rapid BMI growth in childhood is protective for cardiometabolic health.
    BMJ Open 01/2014; 4(4):e004827. · 1.58 Impact Factor
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    ABSTRACT: Social inequalities in overweight and obesity (OWOB) have persisted in the affluent and reputedly egalitarian Nordic countries. In this review we examine associations between socioeconomic position (SEP) and OWOB, and secular trends in such associations. Determinants and possible causes of the relations are discussed together with opportunities to cope with OWOB as a public health problem. The findings show a persisting inverse social gradient. An interaction between SEP and gender is noted for adults in Denmark, Finland and Iceland and for children in Sweden. There are overall tendencies for increased inequality, however no consistent trend for an increased social gradient in OWOB. Reasons that increased inequality does not unequivocally mirror in a steepened social gradient in obesity may include methodological questions as well as societal efforts to counteract obesity. Multi-level efforts are needed to prevent OWOB.
    Current obesity reports. 01/2014; 3:1-15.
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    ABSTRACT: If preschool measures of body size routinely collected at preventive health examinations are associated with adult central obesity and metabolic syndrome, a focused use of these data for the identification of high risk children is possible. The aim of this study was to test the associations between preschool weight and body mass index (BMI) and adult BMI, central obesity and metabolic alterations. The Northern Finland Birth Cohort 1966 (NFBC1966) (N = 4111) is a population-based cohort. Preschool weight (age 5 months and 1 year) and BMI (age 2-5 years) were studied in relation to metabolic syndrome as well as BMI, waist circumference, lipoproteins, blood pressure, and fasting glucose at the age of 31 years. Linear regression models and generalized linear regression models with log link were used. Throughout preschool ages, weight and BMI were significantly linearly associated with adult BMI and waist circumference. Preschool BMI was inversely associated with high-density lipoprotein levels from the age of 3 years. Compared with children in the lower half of the BMI range, the group of children with the 5% highest BMI at the age of 5 years had a relative risk of adult obesity of 6.2(95% CI:4.2-9.3), of adult central obesity of 2.4(95% CI:2.0-2.9), and of early onset adult metabolic syndrome of 2.5(95% CI:1.7-3.8). High preschool BMI is consistently associated with adult obesity, central obesity and early onset metabolic syndrome. Routinely collected measures of body size in preschool ages can help to identify children in need of focused prevention due to their increased risk of adverse metabolic alterations in adulthood.
    PLoS ONE 01/2014; 9(3):e89986. · 3.53 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 01/2014; 9(7):e101134. · 3.53 Impact Factor

Publication Stats

8k Citations
1,817.71 Total Impact Points

Institutions

  • 2012–2014
    • Frederiksberg Hospital
      Фредериксберг, Capital Region, Denmark
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • Aalborg University Hospital
      • Department of Cardiology
      Aalborg, Region North Jutland, Denmark
  • 2006–2014
    • IT University of Copenhagen
      København, Capital Region, Denmark
    • Exiqon
      København, 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
  • 2004–2013
    • University of Southern Denmark
      • Department of Mathematics and Computer Science
      Odense, South Denmark, Denmark
    • Novo Nordisk
      København, Capital Region, Denmark
  • 2002–2013
    • Bispebjerg Hospital, Copenhagen University
      • Institute of Preventive Medicine
      Copenhagen, Capital Region, Denmark
  • 2001–2013
    • Institut for Sygdomsforebyggelse
      København, Capital Region, Denmark
  • 2000–2013
    • Copenhagen University Hospital
      København, Capital Region, Denmark
  • 2007–2012
    • University of Helsinki
      • • Department of Social Research
      • • Department of Oral Medicine
      • • Department of Dental Public Health
      Helsinki, Province of Southern Finland, Finland
    • Glostrup Hospital
      • Department of Ophthalmology
      Copenhagen, Capital Region, Denmark
    • Odense University Hospital
      • Department of Endocrinology - M
      Odense, South Denmark, Denmark
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2011
    • Pierre and Marie Curie University - Paris 6
      Lutetia Parisorum, Île-de-France, France
    • Næstved Hospital
      Нествед, Zealand, Denmark
    • University of Oslo
      Kristiania (historical), Oslo County, Norway
    • National Institute for Public Health and the Environment (RIVM)
      Utrecht, Utrecht, Netherlands
    • The University of Edinburgh
      • Centre for Cognitive Ageing and Cognitive Epidemiology
      Edinburgh, SCT, United Kingdom
  • 2010–2011
    • Imperial College London
      • Department of Epidemiology and Biostatistics
      London, ENG, United Kingdom
    • Roskilde Hospital
      Roskilde, Zealand, Denmark
  • 2009–2011
    • Aarhus University
      • • Department of Clinical Epidemiology
      • • National Centre for Integrated Register-based Research "CIRRAU"
      Aars, Region North Jutland, Denmark
  • 2007–2011
    • Rigshospitalet
      • Department of Paediatrics
      Copenhagen, Capital Region, Denmark
  • 1991–2011
    • Copenhagen University Hospital Hvidovre
      • Department of Clinical Biochemistry
      Hvidovre, Capital Region, Denmark
  • 2008–2009
    • Danish Institute for Health Services Research
      København, Capital Region, Denmark
    • Baylor College of Medicine
      • Department of Pediatrics
      Houston, TX, United States
  • 2003–2009
    • Danish Cancer Society
      København, Capital Region, Denmark
    • Statens Serum Institut
      København, Capital Region, Denmark
    • National Institute of Public Health
      København, Capital Region, Denmark
  • 2001–2009
    • Steno Diabetes Center
      Gjentofte, Capital Region, Denmark
  • 1992–2009
    • University of Copenhagen
      • • Department of Oral Medicine
      • • Faculty of Health and Medical Sciences
      • • Department of Hepatology
      København, Capital Region, Denmark
  • 2006–2007
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark
  • 2005–2007
    • Cornell University
      • Department of Nutritional Sciences
      Ithaca, NY, United States
  • 1980–2006
    • Herlev Hospital
      Herlev, Capital Region, Denmark