A Hofman

Erasmus MC, Rotterdam, South Holland, Netherlands

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Publications (825)5044.27 Total impact

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    ABSTRACT: To assess whether variations in maternal haemoglobin levels during pregnancy are associated with cardio-metabolic risk factors in school age children.
    BJOG An International Journal of Obstetrics & Gynaecology 08/2014; · 3.76 Impact Factor
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    Human Molecular Genetics 08/2014; · 7.69 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWAS) have identified thousands of loci associated with complex traits, but it is challenging to pinpoint causal genes in these loci and to exploit subtle association signals. We used tissue-specific quantitative interaction proteomics to map a network of five genes involved in the Mendelian disorder long QT syndrome (LQTS). We integrated the LQTS network with GWAS loci from the corresponding common complex trait, QT-interval variation, to identify candidate genes that were subsequently confirmed in Xenopus laevis oocytes and zebrafish. We used the LQTS protein network to filter weak GWAS signals by identifying single-nucleotide polymorphisms (SNPs) in proximity to genes in the network supported by strong proteomic evidence. Three SNPs passing this filter reached genome-wide significance after replication genotyping. Overall, we present a general strategy to propose candidates in GWAS loci for functional studies and to systematically filter subtle association signals using tissue-specific quantitative interaction proteomics.
    Nature Methods 08/2014; 11(8):868-74. · 23.57 Impact Factor
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    ABSTRACT: While many neuroimaging studies have investigated the neurobiological basis of attention deficit hyperactivity disorder (ADHD), few have studied the neurobiology of attention problems in the general population. The ability to pay attention falls along a continuum within the population, with children with ADHD at one extreme of the spectrum and, therefore, a dimensional perspective of evaluating attention problems has an added value to the existing literature. Our goal was to investigate the relationship between cortical thickness and inattention and hyperactivity symptoms in a large population of young children.
    Psychological medicine. 07/2014;
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    ABSTRACT: Proprotein convertase subtilisin/kexin-type 1 (PCSK1) activates precursors pro-opiomelanocortin (POMC), proinsulin and prorenin. We investigated if common variants in the PCSK1 gene influence blood pressure and risk of hypertension. Additionally, we investigated the risk of obesity and type 2 diabetes (T2D). In the Rotterdam Study (RS1), a prospective, population-based cohort (n=5974), four single-nucleotide polymorphisms (rs10515237, rs6232, rs436321 and rs3792747) in PCSK1 were studied. Linear and Cox regression models served to analyze associations between variants and end points. Replication was performed in the Rotterdam Study Plus1 (RSPlus1, n=1895). Rs436321 was significantly associated with systolic and diastolic blood pressure and risk of hypertension (odds ratio (OR): 1.1-1.3; P<0.05 in both populations). Rs6232 was associated with body mass index (BMI) (P=0.007 and P=0.04 in RS1 and RSPlus1, respectively). In RSPlus1, heterozygotes for rs6232 had 1.5 times higher risk of obesity (OR: 1.46; 95% confidence interval: 1.04-2.03; P=0.03). We did not find significant associations of PCSK1 with fasting insulin levels and T2D. We found an association of genetic variation in the PCSK1 gene with blood pressure and hypertension. Furthermore, we replicated the association of PCSK1 with BMI and obesity. No relationship was found between PCSK1 variants and fasting insulin levels and T2D. Our findings suggest that genetic variation in PCSK1 may contribute to, at least, some of these interrelated disorders.Journal of Human Hypertension advance online publication, 17 July 2014; doi:10.1038/jhh.2014.59.
    Journal of human hypertension. 07/2014;
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    ABSTRACT: Asthma and chronic obstructive pulmonary disease (COPD) are thought to share a genetic background ("Dutch hypothesis"). We investigated whether asthma and COPD have common underlying genetic factors, performing genome-wide association studies for both asthma and COPD and combining the results in meta-analyses. Three loci showed potential involvement in both diseases: chr2p24.3, chr5q23.1 and chr13q14.2, containing DDX1, COMMD10 (both participating in the nuclear factor (NF) kappabeta pathway) and GNG5P5, respectively. Single nucleotide polymorphisms (SNPs) rs9534578 in GNG5P5 reached genome-wide significance after first replication phase (p = 9.96x10-9). The second replication phase, in seven independent cohorts, provided no significant replication. Expression quantitative trait loci (eQTL) analysis in blood cells and lung tissue on the top 20 associated SNPs identified two SNPs in COMMD10 that influenced gene expression. Inflammatory processes differ in asthma and COPD and are mediated by NF-kappabeta, which could be driven by the same underlying genes, COMMD10 and DDX1. None of the SNPs reached genome-wide significance. Our eQTL studies support a functional role for two COMMD10 SNPs, since they influence gene expression in both blood cells and lung tissue. Our findings suggest that there is either no common genetic component in asthma and COPD or, alternatively, different environmental factors, e.g. lifestyle and occupation in different countries and continents, which may have obscured the genetic common contribution.
    European Respiratory Journal 07/2014; · 6.36 Impact Factor
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    ABSTRACT: Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analysis of FVC in 52,253 individuals from 26 studies and followed up the top associations in 32,917 additional individuals of European ancestry. We found six new regions associated at genome-wide significance (P < 5 x 10(-8)) with FVC in or near EFEMP1, BMP6, MIR129-2-HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease.
    Nature Genetics 07/2014; 46(7):669-77. · 35.21 Impact Factor
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    ABSTRACT: BACKGROUND: Genome-wide association studies (GWAS) have identified numerous loci influencing cross-sectional lung function, but less is known about genes influencing longitudinal change in lung function. METHODS: We performed GWAS of the rate of change in forced expiratory volume in the first second (FEV1) in 14 longitudinal, population-based cohort studies comprising 27,249 adults of European ancestry using linear mixed effects model and combined cohort-specific results using fixed effect meta-analysis to identify novel genetic loci associated with longitudinal change in lung function. Gene expression analyses were subsequently performed for identified genetic loci. As a secondary aim, we estimated the mean rate of decline in FEV1 by smoking pattern, irrespective of genotypes, across these 14 studies using meta-analysis. RESULTS: The overall meta-analysis produced suggestive evidence for association at the novel IL16/STARD5/TMC3 locus on chromosome 15 (P = 5.71 x 10-7). In addition, meta-analysis using the five cohorts with >/=3 FEV1 measurements per participant identified the novel ME3 locus on chromosome 11 (P = 2.18 x 10-8) at genome-wide significance. Neither locus was associated with FEV1 decline in two additional cohort studies. We confirmed gene expression of IL16, STARD5, and ME3 in multiple lung tissues. Publicly available microarray data confirmed differential expression of all three genes in lung samples from COPD patients compared with controls. Irrespective of genotypes, the combined estimate for FEV1 decline was 26.9, 29.2 and 35.7 mL/year in never, former, and persistent smokers, respectively. CONCLUSIONS: In this large-scale GWAS, we identified two novel genetic loci in association with the rate of change in FEV1 that harbor candidate genes with biologically plausible functional links to lung function.
    PLoS ONE 07/2014; 9:e100776. · 3.73 Impact Factor
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    ABSTRACT: Background: Alzheimer’s disease is a common debilitating dementia with known heritability, for which 20 late onset susceptibility loci have been identified, but more remain to be discovered. This study sought to identify new susceptibility genes, using an alternative gene-wide analytical approach which tests for patterns of association within genes, in the powerful genome-wide association dataset of the International Genomics of Alzheimer’s Project Consortium, comprising over 7 m genotypes from 25,580 Alzheimer’s cases and 48,466 controls. Principal Findings: In addition to earlier reported genes, we detected genome-wide significant loci on chromosomes 8 (TP53INP1, p=1.461026) and 14 (IGHV1-67 p=7.961028) which indexed novel susceptibility loci. Significance: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer’s disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimer’s disease
    PLoS ONE 06/2014; 9(6):e94661. · 3.73 Impact Factor
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    ABSTRACT: AimsTo investigate whether polymorphisms in SLC6A20 are associated with susceptibility to Type 2 diabetes.Methods In the Rotterdam Study, a prospective, population-based cohort (n=5974), 22 tagging polymorphisms with minor allele frequencies>0.05 across SLC6A20 were studied. Replication studies were performed in an independent Dutch case–control study (DiaGene-Rotterdam Study 2 n=3133), and in a Chinese Han case–control population (n=2279). A meta-analysis of the results was performed.ResultsIn the Rotterdam study, the minor alleles of rs13062383, rs10461016 and rs2286489 increased the risk of Type 2 diabetes (hazard ratio 1.37, 95% CI 1.15–1.63, hazard ratio 1.30 95% CI 1.09–1.54 and hazard ratio 1.20, 95% CI 1.07–1.35, respectively). In the DiaGene/Rotterdam Study 2, the A allele of rs13062383 increased the risk of Type 2 diabetes (odds ratio 1.45, 95% CI 1.19–1.76). In the Chinese Han study, the rs13062383 A allele also increased the risk of Type 2 diabetes (odds ratio 1.21, 95% CI 1.03–1.42). Meta-analysis showed a highly significant association of rs13062383 with Type 2 diabetes (odds ratio 1.35, 95% CI 1.21–1.47; P=3.3×10-8).Conclusions In conclusion, rs13062383 in SLC6A20 increased the susceptibility to Type 2 diabetes in populations with different genetic backgroundsThis article is protected by copyright. All rights reserved.
    Diabetic Medicine 06/2014; · 3.24 Impact Factor
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    ABSTRACT: Osteoporosis with its consequences, i.e., fractures, is major health problem in ageing societies. As osteoporosis is a prevalent disorder, understanding its etiological factors is very important. We recently identified novel pathogenic variants in PLS3 (encoding Plastin 3 (PLS3), a filamentous-actin bundling protein) as a cause of X-linked osteoporosis and osteoporotic fractures in five Dutch families (van Dijk et al. NEJM 2013:369(16):1529-36). These loss-of-function variants cause decreased bone mineral density and increased risk of fracture in hemizygous young men whereas the clinical picture in heterozygous women ranged from asymptomatic to early-onset osteoporosis. It was highly unexpected that mutations in this gene would cause osteoporosis and fractures as it had never been described as a candidate gene for osteoporosis nor was it known to play a role in bone formation. However, results of in vivo analyses in zebrafish strongly supported a role for PLS3 as a bone regulatory protein. Furthermore, a rare variant (rs140121121) in PLS3 was found to be associated with a twofold increased fracture risk in elderly female carriers in the normal population indicating genetic variation in PLS3 as a novel etiological factor involved in common, multifactorial osteoporosis. However, the exact mechanism by which PLS3 mutations cause osteoporosis and fractures is unknown and currently subject of further investigations. Unravelling this new bone regulatory pathway is of great importance for understanding the aetiology of osteoporosis, increasing also the possibilities for prevention, diagnosis and treatment aimed at bone formation.
    EUROPEAN HUMAN GENETICS CONFERENCE 2014, Milan, Italy; 05/2014
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    ABSTRACT: Background:Breastfeeding duration is associated with the risks of cardio-metabolic diseases in adulthood. We examined the associations of infant feeding patterns with metabolic outcomes in children and whether any association was explained by family-based socio-demographic, maternal lifestyle-related or childhood factors.Subjects/methods:We performed a population-based prospective cohort study in 3417 children to examine the associations of breastfeeding duration and exclusivity and age at introduction of solid foods with blood levels of lipids, insulin and C-peptide and risk of clustering of cardio-metabolic risk factors at the median age of 6.0 years (90% range 5.7-6.8).Results:We observed that, in the models only adjusted for child's age and sex, ever breastfeeding was not associated with childhood blood levels of lipids but was associated with higher insulin and C-peptide concentrations (P-value<0.05). Breastfeeding duration and exclusivity were not consistently associated with metabolic outcomes. Early introduction of solid foods was associated with higher levels of total cholesterol (P-value<0.05) but not with high-density lipoprotein and low-density lipoprotein cholesterol, triglycerides and insulin levels. Shorter breastfeeding duration and exclusive breastfeeding were associated with increased risks of clustering of cardio-metabolic risk factors. After additional adjustment for family, maternal and childhood factors, none of these associations remained significant.Conclusions:In conclusion, we found no consistent associations of infant feeding patterns with metabolic outcomes at school age, after taking into account family-based socio-demographic, maternal lifestyle-related or childhood factors. Whether infant diet composition influences metabolic outcomes in later life should be further studied.European Journal of Clinical Nutrition advance online publication, 30 April 2014; doi:10.1038/ejcn.2014.81.
    European journal of clinical nutrition 04/2014; · 3.07 Impact Factor
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    ABSTRACT: Modulation of dopamine receptor D2 (DRD2) activity affects insulin secretion in both rodents and isolated pancreatic β-cells. We hypothesized that single nucleotide polymorphisms in the DRD2/ANKK1 locus may affect susceptibility to Type 2 diabetes in humans. Four potentially functional variants in the coding region of the DRD2/ANKK1 locus (rs1079597, rs6275, rs6277, rs1800497) were genotyped and analysed for Type 2 diabetes susceptibility in up to 25 000 people (8148 with Type 2 diabetes and 17687 control subjects) from two large independent Dutch cohorts and one Danish cohort. In addition, 340 Dutch subjects underwent a 2-h hyperglycaemic clamp to investigate insulin secretion. Since sexual dimorphic associations related to DRD2 polymorphisms have been previously reported, we also performed a gender-stratified analysis. rs1800497 at the DRD2/ANKK1 locus was associated with a significantly increased risk for Type 2 diabetes in women (odds ratio 1.14 (1.06-1.23); P=4.1*10(-4) ) but not in men (odds ratio 1.00 (95% CI 0.93-1.07); P=0.92) or the combined group. Although rs1800497 was not associated with insulin secretion, we did find another single nucleotide polymorphism in this locus, rs6275, to be associated with increased first-phase glucose-stimulated insulin secretion in women (P=5.5*10(-4) ) but again not in men (P=0.34). The present data identify DRD2/ANKK1 as a potential sex-specific Type 2 diabetes susceptibility gene. This article is protected by copyright. All rights reserved.
    Diabetic Medicine 04/2014; · 3.24 Impact Factor
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    Annals of Neurology 03/2014; · 11.19 Impact Factor
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    ABSTRACT: Background/Objectives:The nutrient-rich food (NRF) index assesses nutrient quality of individual food items by ranking them according to their nutrient composition. The index reflects the nutrient density of the overall diet. We examined the associations between the NRF9.3 index-a score on the basis of nine beneficial nutrients (protein, fiber, vitamins and minerals) and three nutrients to limit (saturated fat, sugar and sodium)-incidence of cardiovascular disease (CVD) events and all-cause mortality.Subjects/Methods:A total of 4969 persons aged 55 and older from the Rotterdam Study, a prospective cohort study in the Netherlands, were studied. First, all foods were scored on the basis of their nutrient composition, resulting in an NRF9.3 score on food item level. Subsequently, they were converted into individual weighted scores on the basis of the amount of calories of each food item consumed by the subjects and the total energy intake. The hazard ratios (HRs) of the NRF9.3 index score were adjusted for age, gender, body mass index, smoking history, doctor-prescribed diet, alcohol consumption and education.Results:Food groups that contributed most to the NRF9.3 index score were vegetables, milk and milk products, fruit, bread and potatoes. A high NRF9.3 index score was inversely associated with all-cause mortality (HR Q4 versus Q1: 0.84 (95% confidence interval: 0.74, 0.96)). Associations were stronger in women than in men. The NRF9.3 index score was not associated with incidence of CVD.Conclusion:Elderly with a higher NRF9.3 index score, indicating more beneficial components and/or less limiting components, had a lower risk of all-cause mortality. Consuming a nutrient-dense diet may improve survival.European Journal of Clinical Nutrition advance online publication, 19 March 2014; doi:10.1038/ejcn.2014.35.
    European journal of clinical nutrition 03/2014; · 3.07 Impact Factor
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    ABSTRACT: To further understanding of the genetic basis of type 2 diabetes (T2D) susceptibility, we aggregated published meta-analyses of genome-wide association studies (GWAS), including 26,488 cases and 83,964 controls of European, east Asian, south Asian and Mexican and Mexican American ancestry. We observed a significant excess in the directional consistency of T2D risk alleles across ancestry groups, even at SNPs demonstrating only weak evidence of association. By following up the strongest signals of association from the trans-ethnic meta-analysis in an additional 21,491 cases and 55,647 controls of European ancestry, we identified seven new T2D susceptibility loci. Furthermore, we observed considerable improvements in the fine-mapping resolution of common variant association signals at several T2D susceptibility loci. These observations highlight the benefits of trans-ethnic GWAS for the discovery and characterization of complex trait loci and emphasize an exciting opportunity to extend insight into the genetic architecture and pathogenesis of human diseases across populations of diverse ancestry.
    Nature Genetics 03/2014; 46(3):234-244. · 35.21 Impact Factor
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    ABSTRACT: The ankle brachial index (ABI) is related to risk of cardiovascular events independent of the Framingham risk score (FRS). The aim of this study was to develop and evaluate a risk model for cardiovascular events incorporating the ABI and FRS. An analysis of participant data from 18 cohorts in which 24,375 men and 20,377 women free of coronary heart disease had ABI measured and were followed up for events. Subjects were divided into a development and internal validation dataset and an external validation dataset. Two models, comprising FRS and FRS + ABI, were fitted for the primary outcome of major coronary events. In predicting events in the external validation dataset, C-index for the FRS was 0.672 (95% CI 0.599 to 0.737) in men and 0.578 (95% CI 0.492 to 0.661) in women. The FRS + ABI led to a small increase in C-index in men to 0.685 (95% CI 0.612 to 0.749) and large increase in women to 0.690 (95% CI 0.605 to 0.764) with net reclassification improvement (NRI) of 4.3% (95% CI 0.0 to 7.6%, p = 0.050) and 9.6% (95% CI 6.1 to 16.4%, p < 0.001), respectively. Restricting the FRS + ABI model to those with FRS intermediate 10-year risk of 10 to 19% resulted in higher NRI of 15.9% (95% CI 6.1 to 20.6%, p < 0.001) in men and 23.3% (95% CI 13.8 to 62.5%, p = 0.002) in women. However, incorporating ABI in an improved newly fitted risk factor model had a nonsignificant effect: NRI 2.0% (95% CI 2.3 to 4.2%, p = 0.567) in men and 1.1% (95% CI 1.9 to 4.0%, p = 0.483) in women. An ABI risk model may improve prediction especially in individuals at intermediate risk and when performance of the base risk factor model is modest.
    European journal of preventive cardiology. 03/2014; 21(3):310-20.
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    ABSTRACT: Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). However, Aβ peptides' functions are not fully understood and seem to be highly pleiotropic. We hypothesized that plasma Aβ peptides concentrations could be a suitable endophenotype for a genome-wide association study (GWAS) designed to (i) identify novel genetic factors involved in amyloid precursor protein metabolism and (ii) highlight relevant Aβ-related physiological and pathophysiological processes. Hence, we performed a genome-wide association meta-analysis of four studies totaling 3 528 healthy individuals of European descent and for whom plasma Aβ1-40 and Aβ1-42 peptides levels had been quantified. Although we did not observe any genome-wide significant locus, we identified 18 suggestive loci (P<1 × 10-5). Enrichment-pathway analyses revealed canonical pathways mainly involved in neuronal functions, for example, axonal guidance signaling. We also assessed the biological impact of the gene most strongly associated with plasma Aβ1-42 levels (cortexin 3, CTXN3) on APP metabolism in vitro and found that the gene protein was able to modulate Aβ1-42 secretion. In conclusion, our study results suggest that plasma Aβ peptides levels are valid endophenotypes in GWASs and can be used to characterize the metabolism and functions of APP and its metabolites.
    Molecular psychiatry 02/2014; · 15.05 Impact Factor
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    ABSTRACT: Specific clusters of metabolic syndrome (MetS) components impact differentially on arterial stiffness, indexed as pulse wave velocity (PWV). Of note, in several population-based studies participating in the MARE (Metabolic syndrome and Arteries REsearch) Consortium the occurrence of specific clusters of MetS differed markedly across Europe and the US. The aim of the present study was to investigate whether specific clusters of MetS are consistently associated with stiffer arteries in different populations. We studied 20,570 subjects from 9 cohorts representing 8 different European countries and the US participating in the MARE Consortium. MetS was defined in accordance with NCEP ATPIII criteria as the simultaneous alteration in ≥3 of the 5 components: abdominal obesity (W), high triglycerides (T), low HDL cholesterol (H), elevated blood pressure (B), and elevated fasting glucose (G). PWV measured in each cohort was "normalized" to account for different acquisition methods. MetS had an overall prevalence of 24.2% (4985 subjects). MetS accelerated the age-associated increase in PWV levels at any age, and similarly in men and women. MetS clusters TBW, GBW, and GTBW are consistently associated with significantly stiffer arteries to an extent similar or greater than observed in subjects with alteration in all the five MetS components - even after controlling for age, sex, smoking, cholesterol levels, and diabetes mellitus - in all the MARE cohorts. In conclusion, different component clusters of MetS showed varying associations with arterial stiffness (PWV).
    Atherosclerosis 01/2014; 233(2):654-660. · 3.71 Impact Factor
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    ABSTRACT: Objective:Fetal smoke exposure may influence growth and body composition later life. We examined the associations of maternal and paternal smoking during pregnancy with total and abdominal fat distribution in school-age children.Methods:We performed a population-based prospective cohort study among 5,243 children followed from early pregnancy onwards in the Netherlands. Information about parental smoking was obtained by questionnaires during pregnancy. At the median age of 6.0 years (90% range 5.7-7.4), we measured anthropometrics, total fat and android/gynoid fat ratio by Dual-energy X-ray absorptiometry, and preperitoneal and subcutaneous abdominal fat measured by ultrasound.Results:The associations of maternal smoking during pregnancy were only present among girls (P-value for sex interaction<0.05). Compared to girls from mothers who did not smoke during pregnancy, those from mothers who smoked during the first trimester only had a higher android/gynoid fat ratio (difference 0.23 (95% Confidence Interval (CI) 0.09-0.37) standard deviation scores (SDS). Girls from mothers who continued smoking throughout pregnancy had a higher body mass index (difference 0.24 (95% CI 0.14-0.35) SDS), total fat mass (difference 0.23 (95% CI 0.14-0.33) SDS), android/gynoid fat ratio (difference 0.34 (95% CI 0.22-0.46) SDS), subcutaneous abdominal fat (difference 0.22 (95% CI 0.11-0.33) SDS), and preperitoneal abdominal fat (difference 0.20 (95% CI 0.08-0.31) SDS). Similar associations with body fat distribution outcomes were observed for paternal smoking during pregnancy. Both continued maternal and paternal smoking during pregnancy may be associated with an increased risk of childhood overweight. The corresponding odds ratios were 1.19 (95% CI 0.98-1.46) and 1.32 (1.10-1.58), respectively.Conclusions:Maternal and paternal smoking during pregnancy are associated with an adverse body and abdominal fat distribution and increased risk of overweight in children. Similar effects of maternal and paternal smoking suggest that direct intrauterine mechanisms and common family based lifestyle-related factors explain the associations.International Journal of Obesity accepted article preview online, 22 January 2014. doi:10.1038/ijo.2014.9.
    International journal of obesity (2005) 01/2014; · 5.22 Impact Factor

Publication Stats

36k Citations
5,044.27 Total Impact Points


  • 1999–2014
    • Erasmus MC
      • • Department of Internal Medicine
      • • Department of Epidemiology
      • • Department of Neurology
      • • Department of Radiology
      Rotterdam, South Holland, Netherlands
  • 1983–2014
    • Erasmus Universiteit Rotterdam
      • • Department of Internal Medicine
      • • Department of Hematology
      • • Department of Ophthalmology
      • • Department of Epidemiology
      Rotterdam, South Holland, Netherlands
  • 2013
    • Uppsala University
      Uppsala, Uppsala, Sweden
  • 1999–2013
    • University Medical Center Utrecht
      • Julius Center for Health Sciences and Primary Care
      Utrecht, Provincie Utrecht, Netherlands
  • 2012
    • Sint Franciscus Gasthuis Rotterdam
      Rotterdam, South Holland, Netherlands
  • 2011
    • King's College London
      • Department of Twin Research and Genetic Epidemiology
      London, ENG, United Kingdom
  • 2009
    • Universitair Ziekenhuis Ghent
      Gand, Flanders, Belgium
  • 1999–2007
    • Universiteit Utrecht
      • Division of Pharmacoepidemiology and Pharmacotherapy
      Utrecht, Provincie Utrecht, Netherlands
  • 2006
    • National Institute on Aging
      Baltimore, Maryland, United States
  • 2003
    • Netherlands Institute for Space Research, Utrecht
      Utrecht, Utrecht, Netherlands
  • 2001
    • Australian National University
      • National Centre for Epidemiology & Population Health Research
      Canberra, Australian Capital Territory, Australia
    • University of Antwerp
      • VIB Department of Molecular Genetics
      Antwerpen, VLG, Belgium
    • University of Groningen
      • Department of Radiology
      Groningen, Province of Groningen, Netherlands
    • St. Paul's Hospital
      Saskatoon, Saskatchewan, Canada
  • 2000
    • University of Münster
      • Institute of Epidemiology and Social Medicine
      Münster, North Rhine-Westphalia, Germany
    • Odense University Hospital
      Odense, South Denmark, Denmark
    • University of Zaragoza
      Caesaraugusta, Aragon, Spain
    • University of Leicester
      Leiscester, England, United Kingdom
    • Karl-Franzens-Universität Graz
      • Section for Neuropsychology
      Graz, Styria, Austria
    • Indiana University-Purdue University Indianapolis
      • Department of Psychiatry
      Indianapolis, IN, United States
  • 1997
    • Leiden University Medical Centre
      Leyden, South Holland, Netherlands
  • 1994
    • Rode Kruis Ziekenhuis Beverwijk
      Berverwyk, North Holland, Netherlands
  • 1990
    • Wageningen University
      • Division of Human Nutrition
      Wageningen, Gelderland, Netherlands
  • 1989
    • Het Oogziekenhuis Rotterdam
      Rotterdam, South Holland, Netherlands