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- King, Sontoria D., et al.
(författare)
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Genetic Susceptibility to Nonalcoholic Fatty Liver Disease and Risk for Pancreatic Cancer: Mendelian Randomization
- 2023
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association For Cancer Research (AACR). - 1055-9965 .- 1538-7755. ; 32:9, s. 1265-1269
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: There are conflicting data on whether nonalcoholic fatty liver disease (NAFLD) is associated with susceptibility to pancreatic cancer. Using Mendelian randomization (MR), we investigated the relationship between genetic predisposition to NAFLD and risk for pancreatic cancer.METHODS: Data from genome-wide association studies (GWAS) within the Pancreatic Cancer Cohort Consortium (PanScan; cases n = 5,090, controls n = 8,733) and the Pancreatic Cancer Case Control Consortium (PanC4; cases n = 4,163, controls n = 3,792) were analyzed. We used data on 68 genetic variants with four different MR methods [inverse variance weighting (IVW), MR-Egger, simple median, and penalized weighted median] separately to predict genetic heritability of NAFLD. We then assessed the relationship between each of the four MR methods and pancreatic cancer risk, using logistic regression to calculate ORs and 95% confidence intervals (CI), adjusting for PC risk factors, including obesity and diabetes.RESULTS: No association was found between genetically predicted NAFLD and pancreatic cancer risk in the PanScan or PanC4 samples [e.g., PanScan, IVW OR, 1.04; 95% confidence interval (CI), 0.88-1.22; MR-Egger OR, 0.89; 95% CI, 0.65-1.21; PanC4, IVW OR, 1.07; 95% CI, 0.90-1.27; MR-Egger OR, 0.93; 95% CI, 0.67-1.28]. None of the four MR methods indicated an association between genetically predicted NAFLD and pancreatic cancer risk in either sample.CONCLUSIONS: Genetic predisposition to NAFLD is not associated with pancreatic cancer risk.IMPACT: Given the close relationship between NAFLD and metabolic conditions, it is plausible that any association between NAFLD and pancreatic cancer might reflect host metabolic perturbations (e.g., obesity, diabetes, or metabolic syndrome) and does not necessarily reflect a causal relationship between NAFLD and pancreatic cancer.
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- D'Onofrio, BM, et al.
(författare)
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Accounting for Confounding in Observational Studies
- 2020
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Ingår i: Annual review of clinical psychology. - : Annual Reviews. - 1548-5951 .- 1548-5943. ; 16, s. 25-48
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Tidskriftsartikel (refereegranskat)abstract
- The goal of this review is to enable clinical psychology researchers to more rigorously test competing hypotheses when studying risk factors in observational studies. We argue that there is a critical need for researchers to leverage recent advances in epidemiology/biostatistics related to causal inference and to use innovative approaches to address a key limitation of observational research: the need to account for confounding. We first review theoretical issues related to the study of causation, how causal diagrams can facilitate the identification and testing of competing hypotheses, and the current limitations of observational research in the field. We then describe two broad approaches that help account for confounding: analytic approaches that account for measured traits and designs that account for unmeasured factors. We provide descriptions of several such approaches and highlight their strengths and limitations, particularly as they relate to the etiology and treatment of behavioral health problems.
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- Oberg, E, et al.
(författare)
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Different sleep pattern in over-weight/obese women with polycystic ovary syndrome
- 2023
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Ingår i: Frontiers in endocrinology. - : Frontiers Media SA. - 1664-2392. ; 14, s. 1068045-
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Tidskriftsartikel (refereegranskat)abstract
- Sleep duration and sleep quality have important health implications although our knowledge of objectively measured sleep variables in women with Polycystic Ovary Syndrome (PCOS) is limited.ObjectiveTo compare sleep variables assessed by actigraphy in over-weight/obese women with PCOS and controls, and to assess sleep variables after behavioral modification intervention in comparison with minimal intervention in a randomized trial.DesignRandomized controlled trial, and a control group.SettingOutpatient gynecological clinic at a university hospital in Sweden.Participants39 women fulfilling all Rotterdam PCOS criteria, randomized to behavioral modification intervention or minimal intervention and 21 controls with no other metabolic disease, all aged 18‐40 years with a BMI ≥ 27 kg/m2.InterventionA four-month behavioral modification intervention including weekly group meetings focusing on behavioral and healthy lifestyle aspects. Minimal intervention reflecting standard care.Main outcome measureSleep durations and sleep efficiency assessed by actigraphy.ResultsCompared to the control group, women with PCOS had significantly shorter time in bed (501 vs 548 min, p= 0.049), sleep time over 24 hours (448 vs 567 min, p=0.005) and sleep time at night (434 vs 511 min, p=0.002), poorer sleep efficiency (87 vs 93%, p<0.001), and longer wakefulness after sleep onset (64 vs 38 min, p<0.001). However, total sleep time at night for women with PCOS (7.2hrs) was within the normal range. Following behavioral modification intervention, the reduction from baseline in sleep over 24 hours and in the daytime sleep were significant compared to the minimal intervention group (78 min, p=0.009 and 43 min, p=0.003 respectively).ConclusionsWe found over-weight/obese women with PCOS to have normal sleep duration, but worse sleep efficiency than controls. Behavioral modification intervention seems to reduce the amount of daytime sleep, suggesting improved sleep behavior.Clinical trials registrationhttps://doi.org/10.1186/ISRCTN48947168, identifier ISRCTN48947168.
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