Piet A van den Brandt

Maastricht Universitair Medisch Centrum, Maestricht, Limburg, Netherlands

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Publications (452)2357.84 Total impact

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    ABSTRACT: Emerging evidence suggests that light physical activity (LPA), besides moderate-to-vigorous physical activity (MVPA), may beneficially influence physical functioning of colorectal cancer survivors, but its relation with other health-related outcomes is unknown. We applied a biopsychosocial approach to investigate independent associations between self-reported LPA, MVPA and multiple health-related quality of life (HRQoL) outcomes in 2-10y post-diagnosis colorectal cancer survivors. Stage I-III colorectal cancer survivors diagnosed between 2002 and 2010 at Maastricht University Medical Center+, the Netherlands, were included in a cross-sectional study (n = 151). Time spent in LPA and MVPA (hours·week), and HRQoL outcome scores (0-100 points) were assessed by validated questionnaires. Median time spent in LPA and MVPA was 10.0 (interquartile range, 2.0-22.0) and 8.7 hours·week (4.5-15.0), respectively. In multivariable linear regression models, both LPA and MVPA were significantly and independently associated with higher physical functioning (mean difference [MD] between highest and lowest quartile, 10.2; 95% CI, 0.2 to 20.3; and 14.5; 5.1 to 23.9, respectively; both P-trend<0.05). Additionally, LPA was significantly associated with higher role functioning (MD, 19.5; 95% CI, 6.9 to 32.1; P-trend<0.01) and lower disability (MD, -9.9; 95% CI, -17.8 to -1.9; P-trend=0.02), independent from MVPA. Subgroup analyses showed that beneficial associations between LPA and HRQoL were mainly observed in women and participants with multiple comorbidities. Self-reported LPA, besides MVPA, was beneficially associated with multiple HRQoL outcomes in colorectal cancer survivors, especially in women and survivors with multiple comorbidities. Prospective studies are warranted to establish whether LPA is a suitable target for personalized lifestyle interventions to improve the HRQoL of colorectal cancer survivors.
    Medicine and science in sports and exercise 05/2015; DOI:10.1249/MSS.0000000000000698 · 4.46 Impact Factor
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    ABSTRACT: Disease classification system increasingly incorporates information on pathogenic mechanisms to predict clinical outcomes and response to therapy and intervention. Technological advancements to interrogate omics (genomics, epigenomics, transcriptomics, proteomics, metabolomics, metagenomics, interactomics, etc.) provide widely open opportunities in population-based research. Molecular pathological epidemiology (MPE) represents integrative science of molecular pathology and epidemiology. This unified paradigm requires multidisciplinary collaboration between pathology, epidemiology, biostatistics, bioinformatics, and computational biology. Integration of these fields enables better understanding of etiologic heterogeneity, disease continuum, causal inference, and the impact of environment, diet, lifestyle, host factors (including genetics and immunity), and their interactions on disease evolution. Hence, the Second International MPE Meeting was held in Boston in December 2014, with aims to: (1) develop conceptual and practical frameworks; (2) cultivate and expand opportunities; (3) address challenges; and (4) initiate the effort of specifying guidelines for MPE. The meeting mainly consisted of presentations of method developments and recent data in various malignant neoplasms and tumors (breast, prostate, ovarian and colorectal cancers, renal cell carcinoma, lymphoma, and leukemia), followed by open discussion sessions on challenges and future plans. In particular, we recognized need for efforts to further develop statistical methodologies. This meeting provided an unprecedented opportunity for interdisciplinary collaboration, consistent with the purposes of the Big Data to Knowledge, Genetic Associations and Mechanisms in Oncology, and Precision Medicine Initiative of the US National Institute of Health. The MPE meeting series can help advance transdisciplinary population science and optimize training and education systems for twenty-first century medicine and public health.
    Cancer Causes and Control 05/2015; DOI:10.1007/s10552-015-0596-2 · 2.96 Impact Factor
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    ABSTRACT: Occupational exposures may be associated with non-vascular dementia. We analyzed the effects of occupational exposures to solvents, pesticides, metals, extremely low frequency magnetic fields (ELF-MF), electrical shocks, and diesel motor exhaust on non-vascular dementia related mortality in the Netherlands Cohort Study (NLCS). Exposures were assigned using job-exposure matrices. After 17.3 years of follow-up, 682 male and 870 female cases were available. Analyses were performed using Cox regression. Occupational exposure to metals, chlorinated solvents and ELF-MF showed positive associations with non-vascular dementia among men, which seemed driven by metals (hazard ratio ever high vs. background exposure: 1.35 [0.98-1.86]). Pesticide exposure showed statistically significant, inverse associations with non-vascular dementia among men. We found no associations for shocks, aromatic solvents, and diesel motor exhaust. Consistent positive associations were found between occupational exposure to metals and non-vascular dementia. The finding on pesticides is not supported in the overall literature. Am. J. Ind. Med. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Industrial Medicine 05/2015; 58(6). DOI:10.1002/ajim.22462 · 1.59 Impact Factor
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    ABSTRACT: In this era of molecular diagnostics, prediction of clear-cell renal cell cancer (ccRCC) survival requires optimization, as current prognostic markers fail to determine individual patient outcome. Epigenetic events are promising molecular markers. Promoter CpG island methylation of cysteine dioxygenase type 1 (CDO1), which was identified as prognostic marker for breast cancer, is studied as potential marker for ccRCC survival. We collected primary tissues of 365 ccRCC cases identified within the prospective Netherlands Cohort Study (NLCS). In this population-based series, CDO1 promoter methylation was observed in 124 of 324 (38.3%) patients with successful methylation-specific PCR analysis. Kaplan-Meier curves and Wilcoxon tests were used to evaluate 10-year ccRCC-specific survival. Cox regression analysis was used to obtain crude and multivariate hazard ratios (HR) and 95% confidence intervals (CI). The relative prognostic value of multivariate models with and without CDO1 promoter methylation was compared using Likelihood-Ratio tests. Patients with CDO1 promoter methylation have a significantly poorer survival than those without (Wilcoxon P=0.006). Differences in survival were independent of other prognostic factors, including age and sex (HR(95%CI)=1.66(1.12-2.45)) and TNM stage, tumor size and Fuhrman grade (HR(95%CI)=1.89(1.25-2.85)). Multivariate models performed better with than without CDO1 promoter methylation status (Likelihood-Ratio P=0.003). Survival curves were validated in an independent series of 280 ccRCC cases from the Cancer Genome Atlas (TCGA; Wilcoxon P<0.001). CDO1 promoter methylation may not substitute common prognostic makers to predict ccRCC survival, but offers additional, relevant prognostic information, indicating that it could be a novel molecular marker to determine ccRCC prognosis. Copyright © 2015, American Association for Cancer Research.
    Clinical Cancer Research 04/2015; DOI:10.1158/1078-0432.CCR-14-2049 · 8.19 Impact Factor
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    ABSTRACT: The International Agency for Research on Cancer (IARC) recently declared air pollution carcinogenic to humans. However, no study of air pollution and lung cancer to date has incorporated adjustment for exposure measurement error, and few have examined specific histological subtypes. Assess the association of air pollution and incident lung cancer in the Netherlands Cohort Study on Diet and Cancer and the impact of measurement error on these associations. The cohort was followed 1986-2003 and 3,355 incident cases were identified. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals, for long-term exposures to NO2, black smoke (BS), PM2.5, and measures of roadway proximity and traffic volume, adjusted for potential confounders. Information from a previous validation study was used to correct the effect estimates for measurement error. We observed elevated risks of incident lung cancer with exposures to BS (HR=1.16, 95% CI: 1.02, 1.32, per 10 µg/m(3)), NO2 (HR=1.29, 95% CI: 1.08, 1.54, per 30 µg/m(3)), PM2.5 (HR=1.17, 95% CI: 0.93, 1.47, per 10 µg/m(3)), and with measures of traffic at the baseline address. The exposures were positively associated with all lung cancer subtypes. After adjustment for measurement error, the HRs increased and the 95% CIs widened (HR=1.19 (95% CI: 1.02, 1.39) for BS and HR=1.37 (95% CI: 0.86, 2.17) for PM2.5). These findings add support to a growing body of literature on the effects of air pollution on lung cancer. In addition, they highlight variation in measurement error by pollutant and support the implementation of measurement error corrections when possible.
    Environmental Health Perspectives 03/2015; DOI:10.1289/ehp.1408762 · 7.03 Impact Factor
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    ABSTRACT: We investigated the association between six occupational exposures (ie, pesticides, solvents, metals, diesel motor emissions (DME), extremely low frequency magnetic fields (ELF-MF) and electric shocks) and Parkinson's disease (PD) mortality in a large population-based prospective cohort study. The Netherlands Cohort Study on diet and cancer enrolled 58 279 men and 62 573 women aged 55-69 years in 1986. Participants were followed up for cause-specific mortality over 17.3 years, until December 2003, resulting in 402 male and 207 female PD deaths. Following a case-cohort design, a subcohort of 5 000 participants was randomly sampled from the complete cohort. Information on occupational history and potential confounders was collected at baseline. Job-exposure matrices were applied to assign occupational exposures. Associations with PD mortality were evaluated using Cox regression. Among men, elevated HRs were observed for exposure to pesticides (eg, ever high exposed, HR 1.27, 95% CI 0.86 to 1.88) and ever high exposed to ELF-MF (HR 1.54, 95% CI 1.00 to 2.36). No association with exposure duration or trend in cumulative exposure was observed for any of the occupational exposures. Results among women were unstable due to small numbers of high-exposed women. Associations with PD mortality were observed for occupational exposure to pesticides and ELF-MF. However, the weight given to these findings is limited by the absence of a monotonic trend with either duration or cumulative exposure. No associations were found between PD mortality and occupational exposure to solvents, metals, DME or electric shocks. 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.
    Occupational and Environmental Medicine 02/2015; DOI:10.1136/oemed-2014-102209 · 3.23 Impact Factor
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    ABSTRACT: Background: The etiology of male breast cancer is poorly understood, partly due to its relative rarity. Although tobacco and alcohol exposures are known carcinogens, their association with male breast cancer risk remains ill-defined. Methods: The Male Breast Cancer Pooling Project consortium provided 2,378 cases and 51,959 controls for analysis from 10 case-control and 10 cohort studies. Individual participant data were harmonized and pooled. Unconditional logistic regression was used to estimate study design-specific (case-control/cohort) odds ratios (OR) and 95% confidence intervals (CI), which were then combined using fixed effects meta-analysis. Results: Cigarette smoking status, smoking pack-years, duration, intensity, and age at initiation were not associated with male breast cancer risk. Relations with cigar and pipe smoking, tobacco chewing, and snuff use were also null. Recent alcohol consumption and average grams of alcohol consumed per day were also not associated with risk; only one sub-analysis of very high recent alcohol consumption (>60 grams/day) was tentatively associated with male breast cancer (ORunexposed referent=1.29, 95%CI:0.97-1.71; OR>0-<7 g/day referent=1.36, 95%CI:1.04-1.77). Specific alcoholic beverage types were not associated with male breast cancer. Relations were not altered when stratified by age or body mass index. Conclusions: In this analysis of the Male Breast Cancer Pooling Project we found little evidence that tobacco and alcohol exposures were associated with risk of male breast cancer. Impact: Tobacco and alcohol do not appear to be carcinogenic for male breast cancer. Future studies should aim to assess these exposures in relation to subtypes of male breast cancer. Copyright © 2014, American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 12/2014; 24(3). DOI:10.1158/1055-9965.EPI-14-1009 · 4.32 Impact Factor
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    ABSTRACT: Nails contain genomic DNA that can be used for genetic analyses, which is attractive for large epidemiologic studies that have collected or are planning to collect nail clippings. Study participants will more readily participate in a study when asked to provide nail samples than when asked to provide a blood sample. In addition, nails are easy and cheap to obtain and store compared with other tissues. We describe our findings on toenail DNA in terms of yield, quality, genotyping a limited set of SNPs with the Sequenom MassARRAY iPLEX platform and high-density genotyping with the Illumina HumanCytoSNP_FFPE-12 DNA array (>262,000 markers). We discuss our findings together with other studies on nail DNA and we compare nails and other frequently used tissue samples as DNA sources. Although nail DNA is considerably degraded, genotyping a limited set of SNPs with the Sequenom MassARRAY iPLEX platform (average sample call rate, 97.1%) and high-density genotyping with the Illumina HumanCytoSNP_FFPE chip (average sample call rate, 93.8%) were successful. Nails are a suitable source of DNA for genotyping in large-scale epidemiologic studies, provided that methods are used that are suitable or optimized for degraded DNA. For genotyping through (next generation) sequencing where DNA degradation is less of an issue, nails may be an even more attractive DNA source, because it surpasses other sources in terms of ease and costs of obtaining and storing the samples. It is worthwhile to consider nails as a source of DNA for genotyping in large-scale epidemiologic studies. See all the articles in this CEBP Focus section, "Biomarkers, Biospecimens, and New Technologies in Molecular Epidemiology." Cancer Epidemiol Biomarkers Prev; 23(12); 2703-12. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 12/2014; 23(12):2703-12. DOI:10.1158/1055-9965.EPI-14-0552 · 4.32 Impact Factor
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    ABSTRACT: The evidence for an association between occupational asbestos exposure and esophageal, gastric and colorectal cancer is limited. We studied this association specifically addressing risk differences between relatively low and high exposure, risk associated with cancer subtypes, the influence of potential confounders, and the interaction between asbestos and smoking in relation to cancer risk. Using the Netherlands Cohort Study (n=58279 men, aged 55-69 years at baseline), asbestos exposure was estimated by linkage to a job-exposure matrix. After 17.3 years of follow-up, 187 esophageal, 486 gastric, and 1724 colorectal cancer cases were available for analysis. The models adjusted for age and family history of cancer showed that mainly (prolonged) exposure to high levels of asbestos was statistically significantly associated with risk of esophageal adenocarcinoma (EAC), total and distal colon cancer, and rectal cancer. For overall gastric cancer and gastric non-cardia adenocarcinoma (GNCA), also exposure to lower levels of asbestos was associated. Additional adjustment for lifestyle confounders, especially smoking status, yielded non-significant associations with overall gastric cancer and GNCA in the multivariable-adjusted model, except for the prolonged highly exposed subjects (tertile 3 vs. never: HR 2.67, 95%CI:1.11-6.44 and HR 3.35, 95%CI:1.33-8.44, respectively). No statistically significant additive or multiplicative interaction between asbestos and smoking was observed for any of the studied cancers. This prospective population-based study showed that (prolonged) high asbestos exposure was associated with overall gastric cancer, EAC, GNCA, total and distal colon cancer, and rectal cancer. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 10/2014; 135(8). DOI:10.1002/ijc.28817 · 5.01 Impact Factor
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    ABSTRACT: Background: Increased oxidative stress has been linked to prostate cancer (PrCa). We investigated oxidative stress-related genetic variants in relation to advanced PrCa risk and examined potential interactions with pro- and antioxidant exposures. Methods: A case-cohort analysis was conducted in the prospective Netherlands Cohort Study, which included 58,279 men aged 55-69 years. Cohort members completed a baseline questionnaire and provided toenail clippings, which were used to isolate DNA. Advanced PrCa cases were identified during 17.3 years of follow-up. The analysis included 14 genetic variants and 11 exposures. Cox regression models were used for analysis and false discovery rate (FDR) Q-values were calculated. Results: Complete genotyping data were available for 952 cases and 1,798 subcohort members. CAT rs1001179 was associated with stage III/IV and stage IV PrCa risk, with HRs per minor allele of 1.16 (95% CI: 1.01-1.33; P=0.032) and 1.25 (95% CI: 1.07-1.46; P=0.006), respectively. We tested 151 gene-environment interactions in relation to both stage III/IV and IV PrCa risk. Seven interactions were statistically significant after adjusting for multiple testing (FDR Q-value <0.20); for stage III/IV PrCa these involved intake of β-carotene (GPX1 rs17650792, hOGG1 rs1052133) and heme iron (GPX1 rs1800668 and rs3448), and for stage IV PrCa these involved intake of catechin (SOD2 rs4880) and heme iron (hOGG1 rs1052133, SOD1 rs10432782). Conclusion: This study of advanced PrCa risk showed a marginal association with a CAT polymorphism and seven novel gene-environment interactions in the oxidative stress pathway. Impact: Oxidative stress-related genes and exposures may have a joint effect on advanced PrCa.
    Cancer Epidemiology Biomarkers & Prevention 10/2014; 24(1). DOI:10.1158/1055-9965.EPI-14-0968 · 4.32 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2198-2198. DOI:10.1158/1538-7445.AM2014-2198 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):1272-1272. DOI:10.1158/1538-7445.AM2014-1272 · 9.28 Impact Factor
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    ABSTRACT: There is limited prospective data on the relationship between consumption of vegetables and fruits and the risk of head-neck cancer (HNC) subtypes (i.e., oral cavity cancer (OCC), oro-/hypopharyngeal cancer (OHPC) and laryngeal cancer (LC)). Therefore, we investigated these associations within the Netherlands Cohort Study, in which 120,852 participants completed a 150-item food frequency questionnaire at baseline in 1986. After 20.3 years of follow-up, 415 cases of HNC (131 OCC, 88 OHPC, 3 oral cavity/pharynx unspecified or overlapping and 193 LC) and 3,898 subcohort members were available for case-cohort analysis using Cox proportional hazards models. Total vegetable and fruit consumption was inversely associated with risk of HNC overall (multivariable-adjusted rate ratios for highest vs. lowest quartile: 0.61, 95% confidence interval (CI) 0.44-0.85, P trend 0.002) and all HNC subtypes, with the strongest associations for OCC. Total vegetable intake and total fruit intake were also associated with a decreased risk of HNC overall and HNC subtypes. No significant interaction was found between vegetable and fruit intake and alcohol consumption or cigarette smoking. In conclusion, in this large-scale cohort study, consumption of vegetables and fruits was associated with a decreased risk of HNC overall and all subtypes. Consumption of vegetables and fruits (or of specific groups of them) may protect against HNC and its subtypes. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 10/2014; DOI:10.1002/ijc.29219 · 5.01 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):5060-5060. DOI:10.1158/1538-7445.AM2014-5060 · 9.28 Impact Factor
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    ABSTRACT: The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on macronutrients, dietary patterns, and risk of adenocarcinoma in Barrett's esophagus; micronutrients, trace elements, and risk of Barrett's esophagus and esophageal adenocarcinoma; the role of mate consumption in the development of squamous cell carcinoma; the relationship between energy excess and development of esophageal adenocarcinoma; and the nutritional management of the esophageal cancer patient.
    Annals of the New York Academy of Sciences 09/2014; 1325(1). DOI:10.1111/nyas.12528 · 4.31 Impact Factor
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    ABSTRACT: Background: Previous epidemiologic research suggests a protective role of one-carbon nutrients in carcinogenesis. Folate, however, may play a dual role in neoplasms development: protect early in carcinogenesis, promote carcinogenesis at a later stage. We prospectively examined associations between intake of total folate, methionine, riboflavin, vitamin B6 and risk of lymphoid and myeloid neoplasms (including subtypes) and investigated whether alcohol modified the effects of folate. Methods: The Netherlands Cohort Study consists of 120,852 individuals who completed a baseline questionnaire in 1986, including a 150-item food-frequency questionnaire. After 17.3 years of follow-up, 1,280 cases of lymphoid and 222 cases of myeloid neoplasms were available for analysis. Results: Intakes of folate, methionine, and riboflavin were not associated with lymphoid or myeloid neoplasms. For vitamin B6, a statistically significantly increased myeloid neoplasms risk was observed (highest versus lowest quintile: HR=1.87, 95%CI=1.08-3.25). When analyzing by lymphoid and myeloid neoplasms subtypes, no clear associations were observed for most subtypes, with just a few increased risks for some subtypes and nutrients. Some risks became non-significant after excluding early cases. No interaction between alcohol and folate was observed. Conclusions: We observed a few significant positive associations; however, some of these would be expected to arise due to chance alone. Furthermore, some risks became non-significant after excluding early cases. Therefore, we conclude that there is no association between one-carbon nutrient intake and risk of lymphoid and myeloid neoplasms. Impact: This study contributes substantially to the limited and inconclusive evidence on the association with one-carbon nutrients.
    Cancer Epidemiology Biomarkers & Prevention 07/2014; 23(10). DOI:10.1158/1055-9965.EPI-14-0136 · 4.32 Impact Factor
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    ABSTRACT: Hypertension is an established risk factor for renal cell cancer (RCC). The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and is closely linked to hypertension. RAAS additionally influences homeostasis of electrolytes (e.g. sodium and potassium) and fluid. We investigated single nucleotide polymorphisms (SNPs) in RAAS and their interactions with hypertension and intakes of sodium, potassium and fluid regarding RCC risk in the Netherlands Cohort Study (NLCS), which was initiated in 1986 and included 120,852 participants aged 55-69 years. Diet and lifestyle were assessed by questionnaires and toenail clippings were collected. Genotyping of toenail DNA was performed using the SEQUENOM® MassARRAY® platform for a literature-based selection of 13 candidate SNPs in seven key RAAS genes. After 20.3 years of follow-up, Cox regression analyses were conducted using a case-cohort approach including 3583 subcohort members and 503 RCC cases. Two SNPs in AGTR1 were associated with RCC risk. AGTR1_rs1492078 (AA vs GG) decreased RCC risk [hazard ratio (HR) (95% confidence interval (CI)): 0.70(0.49-1.00)], whereas AGTR1_rs5186 (CC vs AA) increased RCC risk [HR(95%CI): 1.49(1.08-2.05)]. Associations were stronger in participants with hypertension. The RCC risk for AGT_rs3889728 (AG+AA vs GG) was modified by hypertension (P-interaction=0.039). SNP-diet interactions were not significant, although HRs suggested interaction between SNPs in ACE and sodium intake. SNPs in AGTR1 and AGT influenced RCC susceptibility, and their effects were modified by hypertension. Sodium intake was differentially associated with RCC risk across genotypes of several SNPs, yet some analyses had probably inadequate power to show significant interaction. Results suggest that RAAS may be a candidate pathway in RCC etiology. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 07/2014; DOI:10.1002/ijc.29060 · 5.01 Impact Factor
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    ABSTRACT: Background Metabolomics, defined as the comprehensive identification and quantification of low-molecular-weight metabolites to be found in a biological sample, has been put forward as a potential tool for classifying individuals according to their risk of coronary heart disease (CHD). Here, we investigated whether a single-point blood measurement of the metabolome is associated with and predictive for the risk of CHD. Methods & Results We obtained proton nuclear magnetic resonance (1H-NMR) spectra in 79 cases who developed CHD during follow-up (median 8.1 years) and in 565 randomly selected individuals. In these spectra 100 signals representing 36 metabolites were identified. Applying LASSO regression, we defined a weighted metabolite score consisting of 13 1H-NMR signals that optimally predicted CHD. This metabolite score, including signals representing a lipid fraction, glucose, valine, ornithine, glutamate, creatinine, glycoproteins, citrate and 1.5-anhydrosorbitol, was associated with the incidence of CHD independent of traditional risk factors (TRFs) (HR = 1.50; 95%CI = 1.12-2.01). Predictive performance of this metabolite score on its own was moderate (C-index = 0.75; 95%CI = 0.70-0.80) but after adding age and sex the C-index was only modestly lower than that of TRFs (C-index = 0.81; 95%CI = 0.77-0.85 and C-index = 0.82; 95%CI = 0.78-0.87, respectively). The metabolite score was also associated with prevalent CHD independent of TRFs (OR = 1.59; 95%CI = 1.19-2.13). Conclusion A metabolite score derived from a single-point metabolome measurement is associated with CHD and metabolomics may be a promising tool for refining and improving the prediction of CHD.
    American Heart Journal 07/2014; 168(1). DOI:10.1016/j.ahj.2014.01.019 · 4.56 Impact Factor
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    ABSTRACT: Background: We investigated body size, physical activity, and early life energy restriction in relation to colorectal tumors with and without methylated insulin-like growth factor binding protein (IGFBP) genes, which are putative tumor suppressor genes. Methods: We determined IGFBP2, IGFBP3, and IGFBP7 promoter CpG island hypermethylation in tumors of 733 CRC cases from the Netherlands Cohort Study (N=120,852). Participants self-reported lifestyle and dietary factors at baseline in 1986. Using a case-cohort approach (N subcohort=5,000), we estimated hazard ratios for CRC by extent of IGFBP methylation. Results: Comparison of the highest versus lowest sex-specific tertiles of adult body mass index (BMI) gave multivariable-adjusted hazard ratios (95% confidence intervals (CIs)) for CRCs with 0 (18.7%), 1 (29.5%), 2 (32.4%), and 3 (19.5%) methylated genes of 1.39 (0.88, 2.19), 1.11 (0.77, 1.62), 1.67 (1.17, 2.38), and 2.07 (1.29, 3.33), respectively. Other anthropometric measures and physical activity were not associated with CRC risk by extent of IGFBP methylation, except height in sex-specific analyses for women. Exposure to energy restriction during the Dutch Hunger Winter versus non-exposure gave HRs (95% CIs) for CRCs with 0, 1, 2, and 3 methylated genes of 1.01 (0.67, 1.53), 1.03 (0.74, 1.44), 0.72 (0.52, 0.99), and 0.50 (0.32, 0.78), respectively. Conclusions: Adult BMI, height (in women only), and early life energy restriction were associated with the risk of having a colorectal tumor characterized by IGFBP methylation. Impact: Body size predicts preferentially for IGFBP gene methylated colorectal tumors, which might facilitate more targeted approaches to prevent obesity-related colorectal cancers.
    Cancer Epidemiology Biomarkers & Prevention 06/2014; 23(9). DOI:10.1158/1055-9965.EPI-13-1285 · 4.32 Impact Factor
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    ABSTRACT: The evidence for an association between occupational asbestos exposure and pharyngeal cancer (PhC) is limited, while for oral cavity cancer (OCC) the literature is even sparser. We studied OCC and PhC risk both separately and combined (OCPC) in relation to occupational asbestos exposure, specifically addressing the influence of potential confounders, the existence of an exposure-response relation, and the presence of interaction between asbestos and smoking. Using the prospective Netherlands Cohort Study (N=58 279 men, aged 55-69 years), we estimated asbestos exposure by linkage to a general population job-exposure matrix (DOMJEM) and a Finnish job exposure matrix (FINJEM). After 17.3 years of follow-up, 58 OCC and 53 PhC cases were available for analysis. No association between asbestos and risk of OCC was observed for either JEM. Hazard ratios (HR) of PhC and OCPC increased after adjusting for confounders, particularly alcohol consumption and socioeconomic status. For PhC, a multivariable-adjusted increased HR was observed for "ever" versus "never" exposed to asbestos [HR 2.20, 95% confidence interval (95% CI) 1.08-4.49] when using FINJEM, but a trend of increased risks with higher cumulative exposure could not be demonstrated for either JEM. Results for OCPC showed patterns similar to those observed for PhC. None of the cancers showed a significant interaction between asbestos and smoking. This prospective population-based study showed no convincing evidence of an association between asbestos and risk of OCC, PhC, and OCPC as an exposure-response relation was lacking, and results were not robust against the use of different JEM. However, the potentially increased HR of PhC and OCPC observed in this and previous studies warrant further research.
    Scandinavian Journal of Work, Environment & Health 05/2014; 40(4). DOI:10.5271/sjweh.3434 · 3.10 Impact Factor

Publication Stats

20k Citations
2,357.84 Total Impact Points

Institutions

  • 1997–2015
    • Maastricht Universitair Medisch Centrum
      • Central Diagnostic Laboratory
      Maestricht, Limburg, Netherlands
  • 1990–2015
    • Maastricht University
      • • Department of Epidemiology
      • • GROW School for Oncology & Developmental Biology
      • • CAPHRI School for Public Health and Primary Care
      Maestricht, Limburg, Netherlands
  • 2004–2013
    • University of Toronto
      Toronto, Ontario, Canada
    • CUNY Graduate Center
      New York City, New York, United States
  • 2003–2013
    • Universiteit Utrecht
      • Division of Environmental Epidemiology
      Utrecht, Utrecht, Netherlands
  • 2011
    • Yale University
      New Haven, Connecticut, United States
  • 1998–2008
    • Harvard Medical School
      • • Department of Medicine
      • • Division of Nutrition
      Boston, MA, United States
  • 2007
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 1988–2006
    • TNO
      Delft, South Holland, Netherlands
  • 2005
    • VU University Medical Center
      Amsterdamo, North Holland, Netherlands
  • 2001
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States