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- Fasanelli, Francesca, et al.
(författare)
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Hypomethylation of smoking-related genes is associated with future lung cancer in four prospective cohorts
- 2015
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Ingår i: Nature Communications. - : Nature Publishing Group. - 2041-1723. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- DNA hypomethylation in certain genes is associated with tobacco exposure but it is unknown whether these methylation changes translate into increased lung cancer risk. In an epigenome-wide study of DNA from pre-diagnostic blood samples from 132 case–control pairs in the NOWAC cohort, we observe that the most significant associations with lung cancer risk are for cg05575921 in AHRR (OR for 1 s.d.=0.37, 95% CI: 0.31–0.54, P-value=3.3 × 10−11) and cg03636183 in F2RL3 (OR for 1 s.d.=0.40, 95% CI: 0.31–0.56, P-value=3.9 × 10−10), previously shown to be strongly hypomethylated in smokers. These associations remain significant after adjustment for smoking and are confirmed in additional 664 case–control pairs tightly matched for smoking from the MCCS, NSHDS and EPIC HD cohorts. The replication and mediation analyses suggest that residual confounding is unlikely to explain the observed associations and that hypomethylation of these CpG sites may mediate the effect of tobacco on lung cancer risk.
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| 2. |
- Bould, Helen, et al.
(författare)
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Parental mental illness and eating disorders in offspring
- 2015
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Ingår i: International Journal of Eating Disorders. - : Wiley. - 0276-3478 .- 1098-108X. ; 48:4, s. 383-391
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate which parental mental illnesses are associated with eating disorders in their offspring.METHOD: We used data from a record-linkage cohort study of 158,679 children aged 12-24 years at the end of follow-up, resident in Stockholm County from 2001 to 2007, to investigate whether different parental mental illnesses are risk factors for eating disorders in their offspring. The outcome measure was diagnosis of any eating disorder, either from an ICD or DSM-IV code, or inferred from an appointment at a specialist eating disorder clinic.RESULTS: Mental illness in parents is a risk factor for eating disorders in female offspring (Adjusted Hazard Ratio (AHR) 1.57 (95% CI 1.42, 1.92), p < 0.0001). Risk of eating disorders is increased if there is a parental diagnosis of bipolar affective disorder (AHR 2.28 (95% CI 1.39, 3.72), p = 0.004), personality disorder (AHR 1.57 (95% CI 1.01, 2.44), p = 0.043) or anxiety/depression (AHR 1.57 (95% CI 1.32, 1.86), p < 0.0001). There is a lack of statistical evidence for an association with parental schizophrenia (AHR 1.41 (95% CI 0.96, 2.07), p = 0.08), and somatoform disorder (AHR 1.25 (95% CI 0.74, 2.13), p = 0.40). There is no support for a relationship between parental substance misuse and eating disorders in children (AHR 1.08 (95% CI 0.82, 1.43), p = 0.57).DISCUSSION: Parental mental illness, specifically parental anxiety, depression, bipolar affective disorder, and personality disorders, are risk factors for eating disorders in their offspring.
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| 4. |
- Goetghebeur, Els, et al.
(författare)
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Formulating causal questions and principled statistical answers
- 2020
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Ingår i: Statistics in Medicine. - : WILEY. - 0277-6715 .- 1097-0258. ; 39:30, s. 4922-4948
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Tidskriftsartikel (refereegranskat)abstract
- Although review papers on causal inference methods are now available, there is a lack of introductory overviews onwhatthey can render and on the guiding criteria for choosing one particular method. This tutorial gives an overview in situations where an exposure of interest is set at a chosen baseline ("point exposure") and the target outcome arises at a later time point. We first phrase relevant causal questions and make a case for being specific about the possible exposure levels involved and the populations for which the question is relevant. Using the potential outcomes framework, we describe principled definitions of causal effects and of estimation approaches classified according to whether they invoke the no unmeasured confounding assumption (including outcome regression and propensity score-based methods) or an instrumental variable with added assumptions. We mainly focus on continuous outcomes and causal average treatment effects. We discuss interpretation, challenges, and potential pitfalls and illustrate application using a "simulation learner," that mimics the effect of various breastfeeding interventions on a child's later development. This involves a typical simulation component with generated exposure, covariate, and outcome data inspired by a randomized intervention study. The simulation learner further generates various (linked) exposure types with a set of possible values per observation unit, from which observed as well as potential outcome data are generated. It thus provides true values of several causal effects. R code for data generation and analysis is available on , where SAS and Stata code for analysis is also provided.
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| 7. |
- Mishra, Gita Devi, et al.
(författare)
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Socio-economic position over the life course and all-cause, and circulatory diseases mortality at age 50-87 years : results from a Swedish birth cohort
- 2013
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Ingår i: European Journal of Epidemiology. - : Springer Science and Business Media LLC. - 0393-2990 .- 1573-7284. ; 28:2, s. 139-147
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Tidskriftsartikel (refereegranskat)abstract
- Both child and adult socio-economic position (SEP) predict adult mortality, but little is known about the variation in the impact of SEP across the life course. The Uppsala Birth Cohort Study is a representative birth cohort born 1915–1929 in Uppsala, Sweden. For the 5,138 males and 5,069 females alive in 1980, SEP was available at birth; in adulthood (age 31–45); and in later life (age 51–65). Follow-up for mortality (all-cause, and circulatory disease) was from 1980 to 2002. To test which life course model best described the association between SEP and mortality, we compared the fit of a series of nested Cox proportional hazards regression models (representing either the critical, accumulation or sensitive period models) with a fully saturated model. For all-cause mortality in both genders, the sensitive period model best described the influence of SEP across the life course with a heightened effect in later adult life (males: Hazard Ratio (95 % CI) for advantaged SEP: 0.89 (0.81–0.97) at birth, 0.90 (0.81–0.98) in adulthood, 0.74 (0.67–0.82) in later life; females: 0.87 (0.78–0.98), 0.95 (0.86–1.06), 0.73 (0.64–0.83)). The effect of SEP on circulatory diseases mortality in males was cumulative (HR: 0.84 (0.80–0.87) per unit time in advantaged SEP). For circulatory disease mortality among females, a sensitive period model was selected due to SEP in later adult life (HR: 0.64 (0.52–0.80)). These findings suggest that reducing inequality throughout the life course might reduce all-cause and circulatory disease mortality.
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