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1.
  • Ahrén-Moonga, Jennie, et al. (författare)
  • Association of Higher Parental and Grandparental Education and Higher School Grades With Risk of Hospitalization for Eating Disorders in Females : The Uppsala Birth Cohort Multigenerational Study
  • 2009
  • Ingår i: American Journal of Epidemiology. - 0002-9262 .- 1476-6256. ; 170:5, s. 566-575
  • Tidskriftsartikel (refereegranskat)abstract
    • Eating disorders are a leading cause of disease burden amongyoung women. This study investigated associations of socialcharacteristics of parents and grandparents, sibling position,and school performance with incidence of eating disorders. Theauthors studied Swedish females born in 1952–1989 (n =13,376), third-generation descendants of a cohort born in Uppsalain 1915–1929. Data on grandparental and parental socialcharacteristics, sibling position, school grades, hospitalizations,emigrations, and deaths were obtained by register linkages.Associations with incidence of hospitalization for eating disorderswere studied with multivariable Cox regression, adjusted forage and study period. Overall incidence of hospitalization foreating disorders was 32.0/100,000 person-years. Women with morehighly educated parents and maternal grandparents were at higherrisk (hazard ratio for maternal grandmother with higher educationrelative to elementary education = 6.5, 95% confidence interval:2.2, 19.3, adjusted for parental education). Independent offamily social characteristics, women with the highest schoolgrades had a higher risk of eating disorders (hazard ratio =7.7, 95% confidence interval: 2.5, 24.1 for high compared withlow grades in Swedish, adjusted for parental education). Thus,higher parental and grandparental education and higher schoolgrades may increase risk of hospitalization for eating disordersin female offspring, possibly because of high internal and externaldemands.
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2.
  • Aleksandrova, Krasimira, et al. (författare)
  • Circulating C-reactive protein concentrations and risks of colon and rectal cancer : a nested case-control study within the European Prospective Investigation into Cancer and Nutrition
  • 2010
  • Ingår i: American Journal of Epidemiology. - 0002-9262 .- 1476-6256. ; 172:4, s. 407-418
  • Tidskriftsartikel (refereegranskat)abstract
    • The authors investigated associations between serum C-reactive protein (CRP) concentrations and colon and rectal cancer risk in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (1992-2003) among 1,096 incident cases and 1,096 controls selected using risk-set sampling and matched on study center, age, sex, time of blood collection, fasting status, menopausal status, menstrual cycle phase, and hormone replacement therapy. In conditional logistic regression with adjustment for education, smoking, nutritional factors, body mass index, and waist circumference, CRP showed a significant nonlinear association with colon cancer risk but not rectal cancer risk. Multivariable-adjusted relative risks for CRP concentrations of > or = 3.0 mg/L versus <1.0 mg/L were 1.36 (95% confidence interval (CI): 1.00, 1.85; P-trend = 0.01) for colon cancer and 1.02 (95% CI: 0.67, 1.57; P-trend = 0.65) for rectal cancer. Colon cancer risk was significantly increased in men (relative risk = 1.74, 95% CI: 1.11, 2.73; P-trend = 0.01) but not in women (relative risk = 1.06, 95% CI: 0.67, 1.68; P-trend = 0.13). Additional adjustment for C-peptide, glycated hemoglobin, and high density lipoprotein cholesterol did not attenuate these results. These data provide evidence that elevated CRP concentrations are related to a higher risk of colon cancer but not rectal cancer, predominantly among men and independently of obesity, insulin resistance, and dyslipidemia.
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3.
  • Amirian, E. Susan, et al. (författare)
  • The Glioma International Case-Control Study : A Report From the Genetic Epidemiology of Glioma International Consortium
  • 2016
  • Ingår i: American Journal of Epidemiology. - 0002-9262 .- 1476-6256. ; 183:2, s. 85-91
  • Tidskriftsartikel (refereegranskat)abstract
    • Decades of research have established only a few etiological factors for glioma, which is a rare and highly fatal brain cancer. Common methodological challenges among glioma studies include small sample sizes, heterogeneity of tumor subtypes, and retrospective exposure assessment. Here, we briefly describe the Glioma International Case-Control (GICC) Study (recruitment, 2010-2013), a study being conducted by the Genetic Epidemiology of Glioma International Consortium that integrates data from multiple data collection sites, uses a common protocol and questionnaire, and includes biospecimen collection. To our knowledge, the GICC Study is the largest glioma study to date that includes collection of blood samples, which will allow for genetic analysis and interrogation of gene-environment interactions.
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4.
  • Andersson, Eva M., 1968, et al. (författare)
  • Partial Mediation by Cadmium Exposure of the Association Between Tobacco Smoking and Atherosclerotic Plaques in the Carotid Artery
  • 2018
  • Ingår i: American Journal of Epidemiology. - : Oxford University Press. - 0002-9262 .- 1476-6256. ; 187:4, s. 806-816
  • Tidskriftsartikel (refereegranskat)abstract
    • Exposure to cadmium confers increased cardiovascular risk. Tobacco smoke contains cadmium, which, hypothetically, may mediate parts of the tobacco-associated risk of developing atherosclerotic plaques. Baseline data from the Swedish Malmo Diet and Cancer cohort (1991-1996) were used to test this hypothesis. Mediation analysis was used to examine associations between smoking and blood cadmium levels and the prevalence of ultrasound-assessed carotid atherosclerotic plaques. The total association with smoking status (never smokers, 2 categories of former smokers, and current smokers) was split into direct and indirect association, and the proportion mediated was estimated. The adjusted estimated plaque prevalence was approximately 27% among never smokers. We identified both a direct and an indirect pathway between smoking and carotid plaques; the indirect association, through cadmium, was observed among current smokers and former smokers who had quit smoking less than 15 years before. For current smokers, the prevalence ratio for plaque was 1.5, with 60%-65% of the association with smoking being mediated through cadmium. Recent former smokers had a prevalence ratio of 1.3, and 40%-45% was mediated through cadmium. Long-time former smokers had a prevalence ratio of 1.2, but none of the association was mediated through cadmium. In conclusion, about two-thirds of the proatherosclerotic association with smoking was mediated by cadmium.
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5.
  • Andersson, Kristin, et al. (författare)
  • Prospective Study of Human Papillomavirus Seropositivity and Risk of Nonmelanoma Skin Cancer
  • 2012
  • Ingår i: American Journal of Epidemiology. - : Oxford University Press. - 0002-9262 .- 1476-6256. ; 175:7, s. 685-695
  • Tidskriftsartikel (refereegranskat)abstract
    • Cutaneous human papillomaviruses (HPVs) have been associated with squamous cell carcinoma (SCC) in case-control studies, but there are limited data from prospective studies assessing whether virus exposure predicts risk of future cancer development. Two major biobanks, the Southern Sweden Microbiology Biobank (1971-2003) and the Janus Biobank (1973-2003) in Norway, containing samples from 850,000 donors, were searched for incident skin cancer for up to 30 years using registry linkages. Altogether, 2,623 donors with samples taken before diagnosis of SCC or basal cell carcinoma (BCC) of the skin were identified. Prediagnostic samples and samples from 2,623 matched controls were tested for antibodies against 33 types of HPV. Baseline seropositivity to HPV types in genus beta species 2 was associated with SCC risk (odds ratio = 1.3, 95% confidence interval: 1.1, 1.7); this was also the case for samples taken more than 18 years before diagnosis (odds ratio = 1.8, 95% confidence interval: 1.1, 2.8). Type-specific persistent seropositivity entailed elevated point estimates for SCC risk for 29 HPV types and decreased point estimates for only 3 types. After multiple hypothesis adjustment, HPV 76 was significantly associated with SCC risk and HPV 9 with BCC risk. In summary, seropositivity for certain HPV types was associated with an increased risk for future development of SCC and BCC.
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6.
  • Andersson, Liselott, et al. (författare)
  • Neonatal outcome following maternal antenatal depression and anxiety : a population-based study.
  • 2004
  • Ingår i: American Journal of Epidemiology. - 0002-9262 .- 1476-6256. ; 159:9, s. 872-881
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to determine neonatal outcomes among women who had depressive and anxiety disorders during the second trimester of pregnancy in a population-based sample. Participants were 1,465 women and their neonates born at two obstetric clinics in Sweden. The inclusion period for the women was October 2, 2000-October 1, 2001. The Primary Care Evaluation of Mental Disorders (PRIME-MD) classification system was used to evaluate mental disorders in the second trimester of pregnancy. For assessment of demographic characteristics, birth statistics, and birth-related complications, the medical records of the included women and their offspring were reviewed after delivery. The study results revealed no differences in neonatal outcome between women with antenatal depressive disorders and/or anxiety disorders and healthy subjects. The authors conclude that neonatal outcome did not deteriorate despite the women's impaired mental health during pregnancy.
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7.
  • Arokiasamy, Perianayagam, et al. (författare)
  • Chronic Noncommunicable Diseases in 6 Low-and Middle-Income Countries : Findings From Wave 1 of the World Health Organization's Study on Global Ageing and Adult Health (SAGE)
  • 2017
  • Ingår i: American Journal of Epidemiology. - 0002-9262 .- 1476-6256. ; 185:6, s. 414-428
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper, we examine patterns of self-reported diagnosis of noncommunicable diseases (NCDs) and prevalences of algorithm/measured test-based, undiagnosed, and untreated NCDs in China, Ghana, India, Mexico, Russia, and South Africa. Nationally representative samples of older adults aged >= 50 years were analyzed from wave 1 of the World Health Organization's Study on Global Ageing and Adult Health (2007-2010; n = 34,149). Analyses focused on 6 conditions: angina, arthritis, asthma, chronic lung disease, depression, and hypertension. Outcomes for these NCDs were: 1) self-reported disease, 2) algorithm/measured test-based disease, 3) undiagnosed disease, and 4) untreated disease. Algorithm/measured test-based prevalence of NCDs was much higher than self-reported prevalence in all 6 countries, indicating underestimation of NCD prevalence in low-and middle-income countries. Undiagnosed prevalence of NCDs was highest for hypertension, ranging from 19.7% (95% confidence interval (CI): 18.1, 21.3) in India to 49.6% (95% CI: 46.2, 53.0) in South Africa. The proportion untreated among all diseases was highest for depression, ranging from 69.5% (95% CI: 57.1, 81.9) in South Africa to 93.2% (95% CI: 90.1, 95.7) in India. Higher levels of education and wealth significantly reduced the odds of an undiagnosed condition and untreated morbidity. A high prevalence of undiagnosed NCDs and an even higher proportion of untreated NCDs highlights the inadequacies in diagnosis and management of NCDs in local health-care systems.
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8.
  • Arora, Manish, et al. (författare)
  • An exploration of shared genetic risk factors between periodontal disease and cancers : a prospective co-twin study
  • 2010
  • Ingår i: American Journal of Epidemiology. - Cary, USA : Oxford University Press. - 0002-9262 .- 1476-6256. ; 171:2, s. 253-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Biologic mechanisms underlying associations of periodontal disease with cancers remain unknown. The authors propose that both conditions share common genetic risk factors. They analyzed associations between baseline periodontal disease, measured by questionnaire-recorded tooth mobility, and incident cancers, identified by linkage with national registries, between 1963 and 2004 in 15,333 Swedish twins. The authors used co-twin analyses to control for familial factors and undertook analyses restricted to monozygotic twins to further control for confounding by genetic factors. They observed 4,361 cancer cases over 548,913 person-years. After adjustment for covariates, baseline periodontal disease was associated with increased risk of several cancers ranging from 15% for total cancer (proportional hazard ratio (HR) = 1.15, 95% confidence interval (CI): 1.01, 1.32) to 120% for corpus uterine cancer (HR = 2.20, 95% CI: 1.16, 4.18). Periodontal disease was also associated with increased risk of colorectal (HR = 1.62, 95% CI: 1.13, 2.33), pancreatic (HR = 2.06, 95% CI: 1.14, 3.75), and prostate (HR = 1.47, 95% CI: 1.04, 2.07) cancers. In co-twin analyses, dizygotic twins with baseline periodontal disease showed a 50% increase in total cancer risk (HR = 1.50, 95% CI: 1.04, 2.17), but in monozygotic twins this association was markedly attenuated (HR = 1.07, 95% CI: 0.63, 1.81). Similar patterns emerged for digestive tract cancers, suggesting that shared genetic risk factors may partially explain associations between periodontal disease and cancers.
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9.
  • Baecklund, Fredrik, et al. (författare)
  • Possible Interaction Between Cigarette Smoking and HLA-DRB1 Variation in the Risk of Follicular Lymphoma
  • 2017
  • Ingår i: American Journal of Epidemiology. - : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 185:8, s. 681-687
  • Tidskriftsartikel (refereegranskat)abstract
    • Follicular lymphoma (FL) risk is strongly associated with germline genetic variation in human leukocyte antigen (HLA) class II. Cigarette smoking has been suggested to increase FL risk, primarily among women. We hypothesized that amino acids in HLA-antigen D-related beta 1 subunit (DRB1) interact with smoking in FL risk, as shown for rheumatoid arthritis. We analyzed 373 patients with FL and 818 controls from 2 population-based case-control studies in Sweden and Denmark (1999-2003). Haplotypes in HLA-DRB1 were imputed at amino acid positions 11, 13, 28, 30, and 70-74 (shared epitope). We estimated the relative risk of FL as odds ratios with 95% confidence intervals for different smoking status/haplotype combinations. Interaction was defined as departure from additivity of effects and quantified by the attributable proportion (AP). Relative to never-smokers carrying no shared epitope alleles, smoking was associated with the risk of FL among all subjects (for former smokers, odds ratio (OR) = 2.20, 95% confidence interval (CI): 1.10, 4.41; ORcurrent = 3.56, 95% CI: 1.60, 7.92) and women (ORformer = 2.95, 95% CI: 1.18, 7.37; ORcurrent = 5.63, 95% CI: 2.07, 15.3) carrying 2 shared epitope alleles but not among those carrying zero or 1 shared epitope allele. Smoking and shared epitope status interacted significantly as measured by AP (overall, AP = 0.6, 95% CI: 0.15, 1.0; for women, AP = 0.5, 95% CI: 0.005, 1.0). These results suggest a possible interaction between smoking and HLA-DRB1-associated antigen presentation in FL risk and provide a model to further unravel FL etiology.
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10.
  • Ballin, Marcel, et al. (författare)
  • Cardiovascular Disease and All-Cause Mortality in Male Twins with Discordant Cardiorespiratory Fitness : A Nationwide Cohort Study
  • 2020
  • Ingår i: American Journal of Epidemiology. - : Oxford University Press. - 0002-9262 .- 1476-6256. ; 189:10, s. 1114-1123
  • Tidskriftsartikel (refereegranskat)abstract
    • Whether genetic and familial factors influence the association between cardiorespiratory fitness (CRF) and cardiovascular disease (CVD) is unknown. Two cohorts were formed based on 1,212,295, 18-year-old men that conscripted for military service in Sweden 1972-1996. The first comprised 4,260 twin pairs where twins in each pair had different CRF (≥1 Watt). The second comprised 90,331 non-sibling pairs with different CRF and matched on birth year and year of conscription. Incident CVD and all-cause mortality were identified using national registers. During follow-up (median 32 years), there was no difference in CVD and mortality between fitter twins and less fit twins (246 vs 251 events; hazard ratio [HR] = 1.00, 95% confidence interval [CI]: 0.83, 1.20). The risks were similar in twin pairs with ≥60 Watt difference in CRF (HR = 0.96, 95% CI: 0.57, 1.64). In contrast, in the non-sibling cohort, fitter men had a lower risk of the outcomes than less fit men (4444 vs 5298 events; HR = 0.87, 95% CI: 0.83, 0.92). The association was stronger in pairs with ≥60 Watt difference in CRF (HR = 0.65, 95% CI: 0.59, 0.71). These findings indicate that genetic and familial factors influence the association of CRF with CVD and mortality.
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