Thorkild I A Sørensen

University of Bristol, Bristol, England, United Kingdom

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Publications (608)3440.46 Total impact

  • [Show abstract] [Hide abstract]
    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.
    Environmental Health Perspectives 08/2015; DOI:10.1289/ehp.1409052 · 7.98 Impact Factor
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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.
    BMJ Open 08/2015; 5(8):e008808. DOI:10.1136/bmjopen-2015-008808 · 2.06 Impact Factor
  • Thorkild I.A. Sørensen
    Obesity 07/2015; 23(8). DOI:10.1002/oby.21179 · 4.39 Impact Factor
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    ABSTRACT: Homozygosity has long been associated with rare, often devastating, Mendelian disorders1, and Darwin was one of the first to recognize that inbreeding reduces evolutionary fitness2. However, the effect of the more distant parental relatedness that is common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power3, 4. Here we use runs of homozygosity to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts, and find statistically significant associations between summed runs of homozygosity and four complex traits: height, forced expiratory lung volume in one second, general cognitive ability and educational attainment (P < 1 × 10−300, 2.1 × 10−6, 2.5 × 10−10 and 1.8 × 10−10, respectively). In each case, increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months’ less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing evidence that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples5, 6, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection7, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been.
    Nature 07/2015; DOI:10.1038/nature14618 · 42.35 Impact Factor
  • Peter K. Joshi · Tonu Esko · Hannele Mattsson · Niina Eklund · Ilaria Gandin · Teresa Nutile · Anne U. Jackson · Claudia Schurmann · Albert V. Smith · Weihua Zhang · [...] · Vilmundur Gudnason · Atsushi Takahashi · John C. Chambers · Jaspal S. Kooner · David P. Strachan · Harry Campbell · Joel N. Hirschhorn · Markus Perola · Ozren Polašek · James F. Wilson
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    ABSTRACT: Homozygosity has long been associated with rare, often devastating, Mendelian disorders1, and Darwin was one of the first to recognize that inbreeding reduces evolutionary fitness2. However, the effect of the more distant parental relatedness that is common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power3, 4. Here we use runs of homozygosity to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts, and find statistically significant associations between summed runs of homozygosity and four complex traits: height, forced expiratory lung volume in one second, general cognitive ability and educational attainment (P < 1 × 10−300, 2.1 × 10−6, 2.5 × 10−10 and 1.8 × 10−10, respectively). In each case, increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months’ less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing evidence that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples5, 6, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection7, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been.
    Nature 07/2015; · 42.35 Impact Factor
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    ABSTRACT: Gestational weight gain (GWG) is a complex trait involving intrauterine environmental, maternal environmental, and genetic factors. However, the extent to which these factors contribute to the total variation in GWG is unclear. We therefore examined the genetic and environmental influences on the variation in GWG in the first and second pregnancy in monozygotic (MZ) and dizygotic (DZ) twin mother-pairs. Further, we explored if any co-variance existed between factors influencing the variation in GWG of the mothers' first and second pregnancies. By using Swedish nationwide record-linkage data, we identified 694 twin mother-pairs with complete data on their first pregnancy and 465 twin mother-pairs with complete data on their second pregnancy during 1982-2010. For a subanalysis, 143 twin mother-pairs had complete data on two consecutive pregnancies during the study period. We used structural equation modeling (SEM) to assess the contribution of genetic, shared, and unique environmental factors to the variation in GWG. A bivariate Cholesky decomposition model was used for the subanalysis. We found that genetic factors explained 43% (95% CI: 36-51%) of the variation in GWG in the first pregnancy and 26% (95% CI: 16-36%) in the second pregnancy. The remaining variance was explained by unique environmental factors. Both overlapping and distinct genetic and unique environmental factors influenced GWG in the first and the second pregnancy. This study showed that GWG has a moderate heritability, suggesting that a large part of the variation in the trait can be explained by unique environmental factors.
    Twin Research and Human Genetics 06/2015; DOI:10.1017/thg.2015.38 · 1.92 Impact Factor
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    ABSTRACT: The season of birth might influence prenatal circumstances, which may influence the risk of developing type 2 diabetes. The aim of this study was to determine whether the diagnosis of type 2 diabetes in Denmark changed with the season of birth. This study used data from the population-based Copenhagen School Health Records Register (CSHRR) that includes schoolchildren born between 1930 and 1989. Via a personal identification number, the CSHRR was linked to the National Patient Register containing hospital discharge diagnoses since 1977. The effect of seasonal variation in birth on the risk of type 2 diabetes was assessed using Cox regression, with month or season of birth as the predictor. The underlying time variable was age, and follow-up started in 1977 or at age 30 years. The study population consisted of 223,099 people, of whom 12,486 developed adult type 2 diabetes. Using January as the reference month, the risk of type 2 diabetes by month of birth was not statistically different for any of the 11 comparative birth months. Grouping month of birth into seasons (spring was the reference) gave essentially similar results, showing no difference in the risk of type 2 diabetes for any season. Repeating the analysis by sex, birth cohort and birthweight categories revealed no associations. The risk of adult type 2 diabetes was not associated with month of birth in a large Danish population-based study. The results suggest that the causes of seasonality in birthweight are not causes of type 2 diabetes.
    Diabetologia 06/2015; DOI:10.1007/s00125-015-3661-1 · 6.88 Impact Factor
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    Ramune Jacobsen · Elina Hypponen · Thorkild I. A. Sørensen · Allan A. Vaag · Berit L. Heitmann
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    ABSTRACT: The objective of the study was to assess whether gestational and early infancy exposure to low dose vitamin D from a mandatory margarine fortification programme in Denmark influenced the risk of developing type 1 diabetes (T1D) before age of 15 years. The study population included all individuals born in Denmark from 1983 to 1988 and consisted of 331,623 individuals. The 1st of June 1985, which was the date of issue of the new ministerial order cancelling mandatory fortification of margarine with vitamin D in Denmark, served as a reference point separating the studied population into various exposure groups. We further modelled birth cohort effects in children developing T1D as a linear spline, and compared the slopes between the birth cohorts with various prenatal and infancy exposures to vitamin D fortification. In total, 886 (0.26%) individuals developed T1D before the age of 15 years. The beta coefficients (95% CI), or slopes, for linear birth cohort effect in log Hazard Ratio (HR) per one month of birth in individuals born during the periods of gestational exposure, wash-out, and non-exposure were: 0.010 (-0.002/0.021), -0.010 (-0.035/0.018), and 0.008 (- 0.017/0.032), respectively. The beta coefficients (95% CI) for individuals born during the periods of first postnatal year exposure, wash-out, and non-exposure were: 0.007 (-0.016/0.030), 0.006 (-0.004/0.016), and 0.007 (-0.002/0.016), respectively. In conclusion, we found no evidence to support that exposure to low dose vitamin D from the Danish mandatory margarine fortification regimen during gestational and first postnatal year of life changed the risk of developing T1D before the age of 15 years.
    PLoS ONE 06/2015; 10(6):e0128631. DOI:10.1371/journal.pone.0128631 · 3.23 Impact Factor
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    ABSTRACT: For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m 2 ) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.
    Twin Research and Human Genetics 05/2015; 10(10):1017. DOI:10.1017/thg.2015.29 · 1.92 Impact Factor
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    ABSTRACT: The obesity epidemic may have developed as a response to the obesogenic environment among the genetically predisposed. This investigation examined whether the intergenerational resemblances in childhood overweight changed across the development of the obesity epidemic in groups of children born to parents with and without childhood overweight. The study population was from the Copenhagen School Health Records Register, which includes age- and sex-specific body mass index (BMI; kg/m(2) ) of children. This study used BMI values from 7-year-old children born 1952-1989 and from their parents at ages 7 and 13 years. The available number of parent-child pairs ranged from 17,926 through 42,184. The odds ratios of childhood overweight (BMI z-score >90th percentile) were calculated using logistic regression by parental BMI groups (BMI > or ≤90th percentile) and child birth year intervals. Stable levels in parent-child overweight associations were observed across child BMI groups born to parents with and without childhood overweight. A slight upward odds ratio trend was observed across time in children born to two overweight parents at age 13, but not at age 7 years. Parent-child resemblance in childhood overweight showed small changes during the development of the obesity epidemic, suggesting that the obesogenic environment inducing the epidemic in Denmark influenced children irrespective of their familial predisposition. © 2015 The Obesity Society.
    Obesity 05/2015; 23(6). DOI:10.1002/oby.21060 · 4.39 Impact Factor
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    ABSTRACT: The relation between childhood overweight and adult non-alcoholic fatty liver disease (NAFLD) is largely unknown. We investigated if weight and weight gain in childhood increases the risk of being diagnosed with NAFLD in routine clinical settings in adulthood. We studied 244 464 boys and girls, born between 1930 and 1989, who attended school in Copenhagen, Denmark. Their heights and weights were measured by physicians or nurses at mandatory school health examinations at ages 7-13 years. Body mass index (BMI) z-scores were calculated from an internal age-specific and sex-specific reference. NAFLD reported in the National Patient Register and the National Register of Pathology at 18 years of age or older. HRs with 95% CIs were estimated. During follow-up, 1264 and 1106 NAFLD cases, respectively, occurred in men and women. In both sexes, childhood BMI z-score was not consistently associated with adult NAFLD. Change in BMI z-score between 7 and 13 years of age was positively associated with NAFLD in both sexes. When adjusted for BMI z-score at age 7 years, the HRs of adult NAFLD were 1.15 (95% CI 1.05 to 1.26) and 1.12 (95% CI 1.02 to 1.23) per 1-unit gain in BMI z-score in men and women, respectively. Associations were similar when adjusted for BMI z-score at age 13 years, and were consistent across birth years. A BMI gain in school-aged children is associated with adult NAFLD. Intriguingly, BMI gain appears to have an effect on adult NAFLD irrespective of either the initial or the attained BMI. Taken together, our results suggest that BMI gain in childhood, rather than the level of BMI per se, is important in the development of adult NAFLD. 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.
    BMJ Open 05/2015; 5(4):e006998. DOI:10.1136/bmjopen-2014-006998 · 2.06 Impact Factor
  • International journal of obesity (2005) 04/2015; DOI:10.1038/ijo.2015.81 · 5.39 Impact Factor
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    ABSTRACT: Many environmental factors have been shown to influence birth weight (BW) and one of these are season of birth. The aim of the present study was to investigate the seasonal variation in BW in Denmark during 1936-1989, and to see if the variation could be explained by sunshine exposure during pregnancy. The study population was selected from the Copenhagen School Health Records Register and included 276 339 children born between 1936 and 1989. Seasonal variation was modeled using a non-stationary sinusoidal model that allowed the underlying trend in BW and the amplitude and phase of the yearly cycles to change. There was a clear seasonal pattern in BW which, however, changed gradually across the study period. The highest BWs were seen during fall (September - October) from 1936 to 1963, but a new peak gradually grew from the early 1940s during early summer (May - June) and became the highest from 1964 to 1989. The amplitude of the fall peak started at 25.5 (95%CI 24.6; 25.9) grams and gradually disappeared. The amplitude of the early summer peak gradually arose from nothing to a peak of 18.6 (95%CI 17.7; 19.6) grams in the mid 1980s where it started to decrease again. Sunshine did not explain the seasonal variation in BW. There was a clear seasonal pattern in BW in Denmark 1936-1989, which however changed across the study period. Throughout the study period we observed a peak in BW during the fall, but gradually, starting in the early 1940s, an additional early summer peak emerged and became the highest from 1964 and onwards. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Early human development 04/2015; 91(6):361-365. DOI:10.1016/j.earlhumdev.2015.03.010 · 1.93 Impact Factor
  • C B Jensen · M Gamborg · T L Berentzen · T I A Sørensen · B L Heitmann
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    ABSTRACT: Prenatal vitamin-D deficiency may be associated with increased risk of obesity later in life. Using two national vitamin-D fortification programs as the setting for a societal experiment, we investigated whether exposure to vitamin-D from fortified margarine and low-fat milk during foetal life was associated with body size at 7 years of age. Vitamin-D fortification of margarine was mandatory in Denmark from 1961 to 1985, and voluntary fortification of low-fat milk was permitted from 1972 to 1976. Using information on body mass index (BMI) Z-score at the age of 7 years of 54 270 children, who were measured during the mandatory Copenhagen School Health examination, we compared children according to whether the mothers were pregnant during the fortification programs or not. The comparisons were performed for children born just before and after initiation or termination of margarine and milk fortification periods, respectively. In total four sets of analyses were performed. We observed no difference in mean BMI Z-score between children exposed to vitamin-D fortification in utero and non-exposed children. Similar results were observed for overweight and obesity. Prenatal exposure to vitamin-D from fortification of margarine and low-fat milk showed no association with body size at 7 years.European Journal of Clinical Nutrition advance online publication, 8 April 2015; doi:10.1038/ejcn.2015.55.
    European journal of clinical nutrition 04/2015; DOI:10.1038/ejcn.2015.55 · 2.95 Impact Factor
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    ABSTRACT: Previously, a single nucleotide polymorphism (SNP), rs9939609, in the FTO gene showed a much stronger association with all-cause mortality than expected from its association with body mass index (BMI), body fat mass index (FMI) and waist circumference (WC). This finding implies that the SNP has strong pleiotropic effects on adiposity and adiposity-independent pathological pathways that leads to increased mortality. To investigate this further, we conducted a meta-analysis of similar data from 34 longitudinal studies including 169,551 adult Caucasians among whom 27,100 died during follow-up. Linear regression showed that the minor allele of the FTO SNP was associated with greater BMI (n = 169,551; 0.32 kg m(-2) ; 95% CI 0.28-0.32, P < 1 × 10(-32) ), WC (n = 152,631; 0.76 cm; 0.68-0.84, P < 1 × 10(-32) ) and FMI (n = 48,192; 0.17 kg m(-2) ; 0.13-0.22, P = 1.0 × 10(-13) ). Cox proportional hazard regression analyses for mortality showed that the hazards ratio (HR) for the minor allele of the FTO SNPs was 1.02 (1.00-1.04, P = 0.097), but the apparent excess risk was eliminated after adjustment for BMI and WC (HR: 1.00; 0.98-1.03, P = 0.662) and for FMI (HR: 1.00; 0.96-1.04, P = 0.932). In conclusion, this study does not support that the FTO SNP is associated with all-cause mortality independently of the adiposity phenotypes. © 2015 World Obesity.
    Obesity Reviews 04/2015; 16(4):327-340. DOI:10.1111/obr.12263 · 7.86 Impact Factor
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    ABSTRACT: Objective We studied the influence of maternal behavior on weight change from prepregnancy to 7 years postpartum.Methods We used linear regression to study the independent and combined associations between self-reported behavior in pregnancy (dietary intake, leisure-time exercise, sedentary activity, smoking) and postpartum (breastfeeding duration and smoking) on weights at 6 months, 18 months, and 7 years postpartum.ResultsWomen's average 7-year weight gain was 2.07 kg, with 23% gaining >5 kg. Multivariable analyses suggested that women with healthier dietary intake, more leisure-time exercise, less sedentary behavior, and longer duration of breastfeeding on average gained 1.66 kg [95% confidence interval (CI): 1.40; 1.91] with a significantly reduced odds [OR 0.56 (95% CI: 0.49; 0.64)] of gaining >5 kg from prepregnancy to 7 years postpartum compared to women with none or one of these behaviors [mean gain 3.03 kg (95% CI: 2.68; 3.39)]. Women who ceased smoking had higher long-term weight gain than nonsmokers, but not smokers.Conclusions Adherence to healthy behaviors during pregnancy lowered long-term weight gain considerably by lowering postpartum weight retention and subsequent weight gain. Public health efforts to help mothers achieve healthy behaviors might prevent childbearing-related weight gain.
    Obesity 04/2015; 23(4). DOI:10.1002/oby.21022 · 4.39 Impact Factor
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    ABSTRACT: OBJECTIVES: A trans-ethnic meta-analysis of type 2 diabetes genome-wide association studies has identified seven novel susceptibility variants in or near TMEM154, SSR1/RREB1, FAF1, POU5F1/TCF19, LPP, ARL15 and ABCB9/MPHOSPH9. The aim of our study was to investigate associations between these novel risk variants and type 2 diabetes and pre-diabetic traits in a Danish population-based study with measurements of plasma glucose and serum insulin after an oral glucose tolerance test in order to elaborate on the physiological impact of the variants. METHODS: Case-control analyses were performed in up to 5,777 patients with type 2 diabetes and 7,956 individuals with normal fasting glucose levels. Quantitative trait analyses were performed in up to 5,744 Inter99 participants naïve to glucose-lowering medication. Significant associations between TMEM154-rs6813195 and the beta cell measures insulinogenic index and disposition index and between FAF1-rs17106184 and 2-hour serum insulin levels were selected for further investigation in additional Danish studies and results were combined in meta-analyses including up to 6,486 Danes. RESULTS: We confirmed associations with type 2 diabetes for five of the seven SNPs (TMEM154-rs6813195, FAF1-rs17106184, POU5F1/TCF19-rs3130501, ARL15-rs702634 and ABCB9/MPHOSPH9-rs4275659). The type 2 diabetes risk C-allele of TMEM154-rs6813195 associated with decreased disposition index (n=5,181, β=-0.042, p=0.012) and insulinogenic index (n=5,181, β=-0.032, p=0.043) in Inter99 and these associations remained significant in meta-analyses including four additional Danish studies (disposition index n=6,486, β=-0.042, p=0.0044; and insulinogenic index n=6,486, β=-0.037, p=0.0094). The type 2 diabetes risk G-allele of FAF1-rs17106184 associated with increased levels of 2-hour serum insulin (n=5,547, β=0.055, p=0.017) in Inter99 and also when combining effects with three additional Danish studies (n=6,260, β=0.062, p=0.0040). CONCLUSION: Studies of type 2 diabetes intermediary traits suggest the diabetogenic impact of the C-allele of TMEM154-rs6813195 is mediated through reduced beta cell function. The impact of the diabetes risk G-allele of FAF1-rs17106184 on increased 2-hour insulin levels is however unexplained.
    PLoS ONE 03/2015; 10(3). DOI:10.1371/journal.pone.0120890 · 3.23 Impact Factor
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    Lena Hohwü · Jin Liang Zhu · Lise Graversen · Jiong Li · Thorkild I A Sørensen · Carsten Obel
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    ABSTRACT: Early parental separation may be a stress factor causing a long-term alteration in the hypothalamic-pituitary-adrenal-axis activity possibly impacting on the susceptibility to develop overweight and obesity in offspring. We aimed to examine the body mass index (BMI) and the risk of overweight and obesity in children whose parents lived separately before the child was born. A follow-up study was conducted using data from the Aarhus Birth Cohort in Denmark and included 2876 children with measurements of height and weight at 9-11-years-of-age, and self-reported information on parental cohabitation status at child birth and at 9-11-years-of-age. Quantile regression was used to estimate the difference in median BMI between children whose parents lived separately (n = 124) or together (n = 2752) before the birth. We used multiple logistic regression to calculate odds ratio (OR) for overweight and obesity, adjusted for gender, parity, breast feeding status, and maternal pre-pregnancy BMI, weight gain during pregnancy, age and educational level at child birth; with and without possible intermediate factors birth weight and maternal smoking during pregnancy. Due to a limited number of obese children, OR for obesity was adjusted for the a priori confounder maternal pre-pregnancy BMI only. The difference in median BMI was 0.54 kg/m2 (95% confidence intervals (CI): 0.10; 0.98) between children whose parents lived separately before birth and children whose parents lived together. The risk of overweight and obesity was statistically significantly increased in children whose parents lived separately before the birth of the child; OR 2.29 (95% CI: 1.18; 4.45) and OR 2.81 (95% CI: 1.05; 7.51), respectively. Additional, adjustment for possible intermediate factors did not substantially change the estimates. Parental separation before child birth was associated with higher BMI, and increased risk of overweight and obesity in 9-11-year-old children; this may suggest a fetal programming effect or unmeasured difference in psychosocial factors between separated and non-separated parents.
    PLoS ONE 03/2015; 10(3):e0119138. DOI:10.1371/journal.pone.0119138 · 3.23 Impact Factor
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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; 26(3). DOI:10.1097/EDE.0000000000000261 · 6.18 Impact Factor

Publication Stats

21k Citations
3,440.46 Total Impact Points

Institutions

  • 2015
    • University of Bristol
      Bristol, England, United Kingdom
  • 1977–2015
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 2004–2014
    • Bispebjerg Hospital, Copenhagen University
      • Institute of Preventive Medicine
      København, Capital Region, Denmark
  • 1981–2014
    • Frederiksberg Hospital
      Фредериксберг, Capital Region, Denmark
  • 2006–2013
    • University of Copenhagen
      • Faculty of Health and Medical Sciences
      Copenhagen, Capital Region, 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
  • 2002–2011
    • Statens Serum Institut
      • Department of Epidemiology Research
      København, Capital Region, Denmark
    • Laval University
      Quebec City, Quebec, Canada
  • 2010
    • Technical University of Denmark
      Lyngby, Capital Region, Denmark
  • 2009
    • Danish Institute for Health Services Research
      København, Capital Region, Denmark
  • 1985–2009
    • University of Helsinki
      • Department of Dental Public Health
      Helsinki, Province of Southern Finland, Finland
  • 1997–2008
    • Steno Diabetes Center
      Gjentofte, Capital Region, Denmark
  • 2007
    • University of Oulu
      Uleoborg, Northern Ostrobothnia, Finland
    • Odense University Hospital
      • Department of Endocrinology - M
      Odense, South Denmark, Denmark
  • 2005–2007
    • Cornell University
      • Department of Nutritional Sciences
      Ithaca, NY, United States
  • 2003–2005
    • Aarhus University
      • Department of Epidemiology and Social Medicine
      Aarhus, Central Jutland, Denmark
  • 2003–2004
    • National Institute of Public Health
      København, Capital Region, Denmark
  • 1979–2003
    • 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
    • William Penn University
      Filadelfia, Pennsylvania, United States
  • 1989–1991
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1983–1987
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark