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Sökning: WFRF:(Mariosa Daniela)

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1.
  • Andersen, Kasper, 1974-, et al. (författare)
  • Dose–Response Relationship of Total and Leisure Time Physical Activity to Risk of Heart Failure : a prospective cohort study
  • 2014
  • Ingår i: Circulation Heart Failure. - 1941-3289 .- 1941-3297. ; 7:5, s. 701-708
  • Tidskriftsartikel (refereegranskat)abstract
    • Background—The nature of the association between levels of physical activity and risk of heart failure is little known. We investigated nonlinear associations of total and leisure time physical activity with risk of heart failure.Methods and Results—In 1997, 39 805 persons without heart failure completed a questionnaire of lifestyle factors and medical history. We used Cox regression models to investigate total (adjusting for education and previous myocardial infarction) and direct (multivariable-adjusted) effects of self-reported total and leisure time physical activity on risk of heart failure of any cause and heart failure of nonischemic origin. Heart failure diagnoses were obtained until December 31, 2010. Higher leisure time physical activity was associated with lower risk of heart failure of any cause; hazard ratio of the total effect of leisure time physical activity was for fifth versus first quintile 0.54; 95% confidence interval was 0.44 to 0.66. The direct effect was similar. High total daily physical activity level was associated with lower risk of heart failure, although the effect was less pronounced than for leisure time physical activity (total effect hazard ratio, 0.81; 95% confidence interval, 0.69–0.95; fifth versus first quintile). A similar direct effect observed.Conclusions—Leisure time physical activity was inversely related to risk of developing heart failure in a dose–response fashion. This was reflected in a similar but less pronounced association of total physical activity with risk of heart failure. Only part of the effects appeared to be mediated by traditional risk factors.
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2.
  • Grotta, Alessandra, et al. (författare)
  • Physical activity and body mass index as predictors of prostate cancer risk
  • 2015
  • Ingår i: World journal of urology. - 0724-4983 .- 1433-8726. ; 33:10, s. 1495-1502
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: Physical activity and body mass index (BMI) are involved in prostate cancer etiology; possible biologic mechanisms include their effects on hormonal levels. Our aim was to investigate the relationship between physical activity, obesity, and prostate cancer.METHODS: We followed a cohort of 13,109 Swedish men for 13 years and investigated the association of self-reported physical activity and BMI at baseline with prostate cancer incidence. We further analyzed whether BMI could modulate effects of physical activity. Occupational, recreational, and total physical activity were analyzed in relation to overall, localized, and advanced prostate cancer.RESULTS: During the study follow-up, we observed a total of 904 cases of prostate cancer (429 localized, 407 advanced, and 68 unclassified). High levels of occupational physical activity were associated with a nonsignificantly decreased risk of overall (HR 0.81, 95 % CI 0.61-1.07), localized (HR 0.75, 95 % CI 0.51-1.12), and advanced (HR 0.85, 95 % CI 0.55-1.31) prostate cancer. We found no association between high BMI and risk of prostate cancer incidence: We observed, however, a significant interaction between BMI and leisure physical activity.CONCLUSION: No association was confirmed between total physical activity and localized or advanced prostate cancer. The highest, relative to the lowest, level of occupational physical activity tended to be linked to a lower risk of prostate cancer, with a suggested dose-response relationship. We found no association between high BMI and risk of prostate cancer incidence; however, our analyses suggested an interaction between BMI and physical activity during recreational time that merits further investigation in future studies.
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3.
  • Johansson, Mattias, et al. (författare)
  • The influence of obesity-related factors in the etiology of renal cell carcinoma—A mendelian randomization study
  • 2019
  • Ingår i: ; 16:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several obesity-related factors have been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directly influence risk. We addressed this question using genetic markers as proxies for putative risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework. This methodology limits bias due to confounding and is not affected by reverse causation.Methods and findings: Genetic markers associated with obesity measures, blood pressure, lipids, type 2 diabetes, insulin, and glucose were initially identified as instrumental variables, and their association with RCC risk was subsequently evaluated in a genome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-sample MR framework. The effect on RCC risk was estimated by calculating odds ratios (ORSD) for a standard deviation (SD) increment in each risk factor. The MR analysis indicated that higher body mass index increases the risk of RCC (ORSD: 1.56, 95% confidence interval [CI] 1.44–1.70), with comparable results for waist-to-hip ratio (ORSD: 1.63, 95% CI 1.40–1.90) and body fat percentage (ORSD: 1.66, 95% CI 1.44–1.90). This analysis further indicated that higher fasting insulin (ORSD: 1.82, 95% CI 1.30–2.55) and diastolic blood pressure (DBP; ORSD: 1.28, 95% CI 1.11–1.47), but not systolic blood pressure (ORSD: 0.98, 95% CI 0.84–1.14), increase the risk for RCC. No association with RCC risk was seen for lipids, overall type 2 diabetes, or fasting glucose.Conclusions: This study provides novel evidence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and DBP influence RCC risk.
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4.
  • Longinetti, Elisa, et al. (författare)
  • Neurodegenerative and psychiatric diseases among families with amyotrophic lateral sclerosis
  • 2017
  • Ingår i: ; 89:6, s. 578-585
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To estimate risks of neurodegenerative and psychiatric diseases among patients with amyotrophic lateral sclerosis (ALS) and their families.Methods: We conducted a register-based nested case-control study during 1990-2013 in Sweden to assess whether patients with ALS had higher risks of other neurodegenerative and psychiatric diseases before diagnosis. We included 3,648 patients with ALS and 36,480 age-, sex-, and county of birth-matched population controls. We further conducted a follow-up study of the cases and controls to assess the risks of other neurodegenerative and psychiatric diseases after ALS diagnosis. To assess the potential contribution of familial factors, we conducted similar studies for the relatives of patients with ALS and their controls.Results: Individuals with previous neurodegenerative or psychiatric diseases had a 49% increased risk of ALS (odds ratio 1.49, 95% confidence interval 1.35-1.66) compared to individuals without these diseases. After diagnosis, patients with ALS had increased risks of other neurodegenerative or psychiatric diseases (hazard ratio 2.90, 95% confidence interval 2.463.43) compared to individuals without ALS. The strongest associations were noted for frontotemporal dementia, Parkinson disease, other dementia, Alzheimer disease, neurotic disorders, depression, stress-related disorders, and drug abuse/dependence. First-degree relatives of patients with ALS had higher risk of neurodegenerative diseases, whereas only children of patients with ALS had higher risk of psychiatric disorders, compared to relatives of the controls.Conclusions: Familial aggregation of ALS and other neurodegenerative diseases implies a shared etiopathogenesis among all neurodegenerative diseases. The increased risk of psychiatric disorders among patients with ALS and their children might be attributable to nonmotor symptoms of ALS and severe stress response toward the diagnosis.
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5.
  • Mariosa, Daniela, et al. (författare)
  • Antidiabetics, Statins, and the Risk of Amyotrophic Lateral Sclerosis
  • 2020
  • Ingår i: ; 27:6, s. 1010-1016
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Medications that are used for treatment of metabolic disorders have been suggested to be associated with the development of amyotrophic lateral sclerosis (ALS).METHODS: To examine the associations of antidiabetics and statins with the subsequent risk of ALS we conducted a population-based nested case-control study of 2,475 Swedish residents diagnosed with ALS during July 2006-December 2013, and 12,375 population controls (five for each ALS case). We extracted from the Swedish Prescribed Drug Register information on filled prescriptions of antidiabetics and statins for both cases and controls during the years before ALS diagnosis. Conditional logistic regression was used to calculate odds ratios (ORs) for the associations of these medications with ALS risk.RESULTS: ALS patients were less likely to have been prescribed with antidiabetics, compared to controls (OR=0.76, 95%CI=0.65-0.90). Conversely, statins were not associated with ALS risk overall (OR=1.08, 95%CI=0.98-1.19), although a positive association was noted among women (OR=1.28, 95%CI=1.10-1.48). The latter association was mostly explained by ALS cases being more likely to have a first prescription of statins during the year before diagnosis, compared to controls (OR=2.54, 95%CI=1.84-3.49).CONCLUSIONS: The inverse association of antidiabetics with ALS is consistent with the previously reported inverse association between type 2 diabetes and ALS risk. The increase in prescription of statins during the year before ALS diagnosis deserves attention because it might reflect an acceleration of the course of ALS due to statin use.
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6.
  • Sun, Jiangwei, et al. (författare)
  • Antibiotics Use and Risk of Amyotrophic Lateral Sclerosis in Sweden
  • 2019
  • Ingår i: European Journal of Neurology. - : Blackwell Publishing. - 1351-5101 .- 1468-1331. ; 26:11, s. 1355-1361
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: Previous animal studies have suggested disrupted intestinal microbiome in amyotrophic lateral sclerosis (ALS). Due to the known effect of antibiotics on gut microflora, the potential role of antibiotics use on the risk of ALS deserves an investigation.METHODS: A nested case-control study was conducted using several Swedish national registers. We included 2,484 ALS patients diagnosed between July 1, 2006 and December 31, 2013 as cases and randomly selected five controls per case who were individually matched to the case by sex, birth year, and area of residence from the general Swedish population. Information on antibiotics prescriptions before ALS diagnosis was extracted from the Prescribed Drug Register for both cases and controls. Conditional logistic regression model was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).RESULTS: After accounting for potential diagnostic delay in ALS by excluding all prescriptions within one year before diagnosis, any antibiotics use was associated with a higher risk of ALS. The ORs (95% CIs) were 1.06 (0.94-1.19), 1.13 (1.00-1.28), and 1.18 (1.03-1.35) when comparing one, 2-3, and ≥4 prescriptions to no prescription (P for trend = 0.0069). Similar results were noted for antibiotics used for respiratory infections and urinary tract as well as skin and soft tissue infections. Among different individual antibiotics, the risk of ALS was especially increased in relation to more than two prescriptions of beta-lactamase sensitive penicillin (OR=1.28; 95% CI 1.10-1.50).CONCLUSIONS: Use of antibiotics, especially repeated, might be associated with a higher subsequent risk of ALS.
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7.
  • Johansson, Mattias, et al. (författare)
  • The influence of obesity-related factors in the etiology of renal cell carcinoma : A mendelian randomization study
  • 2019
  • Ingår i: ; 16:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several obesity-related factors have been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directly influence risk. We addressed this question using genetic markers as proxies for putative risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework. This methodology limits bias due to confounding and is not affected by reverse causation.Methods and findings: Genetic markers associated with obesity measures, blood pressure, lipids, type 2 diabetes, insulin, and glucose were initially identified as instrumental variables, and their association with RCC risk was subsequently evaluated in a genome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-sample MR framework. The effect on RCC risk was estimated by calculating odds ratios (ORSD) for a standard deviation (SD) increment in each risk factor. The MR analysis indicated that higher body mass index increases the risk of RCC (ORSD: 1.56, 95% confidence interval [CI] 1.44–1.70), with comparable results for waist-to-hip ratio (ORSD: 1.63, 95% CI 1.40–1.90) and body fat percentage (ORSD: 1.66, 95% CI 1.44–1.90). This analysis further indicated that higher fasting insulin (ORSD: 1.82, 95% CI 1.30–2.55) and diastolic blood pressure (DBP; ORSD: 1.28, 95% CI 1.11–1.47), but not systolic blood pressure (ORSD: 0.98, 95% CI 0.84–1.14), increase the risk for RCC. No association with RCC risk was seen for lipids, overall type 2 diabetes, or fasting glucose.Conclusions: This study provides novel evidence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and DBP influence RCC risk.
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8.
  • Mariosa, Daniela (författare)
  • Metabolic disorders in the etiology of amyotrophic lateral sclerosis : an epidemiological approach
  • 2017
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a loss of motor neurons in the brain and spinal cord, leading to progressive muscle weakness in multiple regions of the body. No effective treatment is available and the disease progresses rapidly to death with an average survival time of 3-5 years after symptom onset. The etiology of ALS is unknown for the majority of the patients. Alterations in the carbohydrate and lipid metabolisms, together with hypermetabolism, are features of ALS patients that are not yet well characterized. Understanding the early metabolic symptoms of the disease might be a necessary step for the identification of an effective treatment. Paper I describes a nested case-control study on the association between diabetes and the future risk of ALS in the Swedish population. A total of 5,108 new ALS cases among the Swedish residents between 1991 and 2010 were identified from the National Patient Register. Through linkages to several nationwide Swedish registers five controls per case were selected from the entire Swedish population using incidence density sampling and diabetes diagnoses were identified for both cases and controls from hospital admission records, outpatient care records, prescription of antidiabetics, or a combination of the three. An overall inverse association between diabetes and risk of ALS was found. There was however a positive association between insulin-dependent diabetes before age 30 and ALS risk. Paper II describes the association between body mass index (BMI), BMI change and ALS risk and survival in the GENEVA study, a case-control study of United States military veterans. Self-reported BMI at age 25, 40 and at time of ALS diagnosis (interview for controls) was compared. Low BMI at age 40 was associated with increased risk of developing ALS and the association was stronger for cases with diagnostic delay shorter than one year. Stable or decreasing BMI between age 25 and 40 was also associated with higher risk of ALS compared to an increasing BMI. However, premorbid BMI and BMI change did not predict survival of ALS patients. Paper III describes the association between ALS risk and serum glucose, total cholesterol, LDL-C, HDL-C, triglycerides, apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I) in a Swedish populationbased cohort study. High LDL-C, apoB and the LDL-C/HDL-C and apoB/apoA-I ratios were associated with a higher incidence of ALS. These associations seemed to be mainly due to a strong association of apoB with ALS risk. High glucose level ( 6.11 mmol/L) was associated with a lower incidence of ALS. During the 10 years before diagnosis, ALS patients had increasing levels of LDL-C, HDL-C, apoB and apoA-I, whereas gradually decreasing levels of LDL-C/HDL-C and apoB/apoA-I ratios. Paper IV describes a population-based nested case-control study of 2,475 Swedish residents diagnosed with ALS during July 2006-December 2013, and 12,375 population controls. Information on filled prescriptions of antidiabetics and statins were extracted from the Swedish Prescribed Drug Register. Antidiabetics were associated with a lower ALS risk, the association was stronger for men, for individuals above age 65, and for ALS with longer disease duration. Statins were not associated with ALS risk overall, though a positive association was noted among women. The latter association was mostly explained by increased statins use during the year before ALS diagnosis. The studies presented in this thesis have taken advantage of different study designs and populations to systematically investigate the relationship between metabolic disorders and ALS risk and, to a lesser extent, progression. Therefore, they contributed substantially to fill the knowledge gap about the association between metabolic disorders and neurodegeneration in ALS. Furthermore, Paper I and Paper IV serve as excellent examples of the unique possibilities offered by the nationwide health registers in Sweden that can, when equipped with modern analytical methods, contribute to the understanding of complex diseases.
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