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Pell, Jill P. - One of the best experts on this subject based on the ideXlab platform.
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The associations of sugar-sweetened, artificially sweetened and naturally sweet juices with all-cause mortality in 198,285 UK Biobank participants: a prospective cohort study
BMC, 2020Co-Authors: Anderson, Jana J., Gray, Stuart R, Welsh Paul, Mackay, Daniel F., Celis-morales, Carlos A., Lyall, Donald M., Forbes, John F., Sattar Naveed, Gill, Jason M. R., Pell, Jill P.Abstract:Background: Recent efforts to address the obesity epidemic have focused on sugar consumption, especially sugar-sweetened beverages. However, sugar takes many forms, is only one contributor to overall energy consumption and is correlated with other health-related lifestyle factors. The objective was to investigate the associations with allcause mortality of sugar- and artificially sweetened beverages and naturally sweet juices. Methods: Setting: UK Biobank, UK. Participants joined the UK Biobank study from 2006 to 2010 and were followed up until 2016; 198,285 men and women aged 40–69 years were eligible for this study (40% of the UK Biobank), of whom 3166 (1.6%) died over a mean of 7 years follow-up. Design: prospective population-based cohort study. Exposure variables: dietary consumption of sugar-sweetened beverages, artificially sweetened beverages, naturally sweet juices (100% fruit/vegetable juices) and total sugar intake, self-reported via 24-h dietary assessment tool completed between 2009 and 2012. Main outcome: all-cause mortality. Cox regression analyses were used to study the association between the daily intake of the above beverages and all-cause mortality. Models were adjusted for socio-demographic, economic, lifestyle and dietary confounders. Results: Total energy intake, total sugar intake and percentage of energy derived from sugar were comparable among participants who consumed > 2/day sugar-sweetened beverages and > 2/day fruit/vegetable juices (10,221 kJ/day versus 10,381 kJ/day; 183 g versus 190 g; 30.6% versus 31.0%). All-cause mortality was associated with total sugar intake (highest quintile adj. HR 1.28, 95% CI 1.06–1.55) and intake of sugar-sweetened beverages (> 2/day adj. HR 1.84, 95% CI 1.42–2.37) and remained so in sensitivity analyses. An association between artificially sweetened beverage intake and mortality did not persist after excluding deaths in the first 2 years of follow-up (landmark analysis) nor after excluding participants with recent weight loss. Furthermore, the inverse association between fruit/vegetable juice intake and mortality did not persist after additional adjustment for a diet quality score. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation
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The associations of sugar-sweetened, artificially sweetened and naturally sweet juices with all-cause mortality in 198,285 UK Biobank participants: a prospective cohort study
'Springer Science and Business Media LLC', 2020Co-Authors: Anderson, Jana J., Gray, Stuart R, Welsh Paul, Mackay, Daniel F., Celis-morales, Carlos A., Lyall, Donald M., Forbes, John F., Sattar Naveed, Gill, Jason M. R., Pell, Jill P.Abstract:peer-reviewedBackground: Recent efforts to address the obesity epidemic have focused on sugar consumption, especially sugar-sweetened beverages. However, sugar takes many forms, is only one contributor to overall energy consumption and is correlated with other health-related lifestyle factors. The objective was to investigate the associations with allcause mortality of sugar- and artificially sweetened beverages and naturally sweet juices. Methods: Setting: UK Biobank, UK. Participants joined the UK Biobank study from 2006 to 2010 and were followed up until 2016; 198,285 men and women aged 40–69 years were eligible for this study (40% of the UK Biobank), of whom 3166 (1.6%) died over a mean of 7 years follow-up. Design: prospective population-based cohort study. Exposure variables: dietary consumption of sugar-sweetened beverages, artificially sweetened beverages, naturally sweet juices (100% fruit/vegetable juices) and total sugar intake, self-reported via 24-h dietary assessment tool completed between 2009 and 2012. Main outcome: all-cause mortality. Cox regression analyses were used to study the association between the daily intake of the above beverages and all-cause mortality. Models were adjusted for socio-demographic, economic, lifestyle and dietary confounders. Results: Total energy intake, total sugar intake and percentage of energy derived from sugar were comparable among participants who consumed > 2/day sugar-sweetened beverages and > 2/day fruit/vegetable juices (10,221 kJ/day versus 10,381 kJ/day; 183 g versus 190 g; 30.6% versus 31.0%). All-cause mortality was associated with total sugar intake (highest quintile adj. HR 1.28, 95% CI 1.06–1.55) and intake of sugar-sweetened beverages (> 2/day adj. HR 1.84, 95% CI 1.42–2.37) and remained so in sensitivity analyses. An association between artificially sweetened beverage intake and mortality did not persist after excluding deaths in the first 2 years of follow-up (landmark analysis) nor after excluding participants with recent weight loss. Furthermore, the inverse association between fruit/vegetable juice intake and mortality did not persist after additional adjustment for a diet quality score. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation
George Davey Smith - One of the best experts on this subject based on the ideXlab platform.
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causal inference in cancer epidemiology what is the role of mendelian randomization
Cancer Epidemiology Biomarkers & Prevention, 2018Co-Authors: James Yarmolinsky, George Davey Smith, Kaitlin H Wade, Caroline L Relton, Rebecca C Richmond, Ryan Langdon, Caroline J Bull, Kate Tilling, Sarah J Lewis, Richard M MartinAbstract:Observational epidemiologic studies are prone to confounding, measurement error, and Reverse Causation, undermining robust causal inference. Mendelian randomization (MR) uses genetic variants to proxy modifiable exposures to generate more reliable estimates of the causal effects of these exposures on diseases and their outcomes. MR has seen widespread adoption within cardio-metabolic epidemiology, but also holds much promise for identifying possible interventions for cancer prevention and treatment. However, some methodologic challenges in the implementation of MR are particularly pertinent when applying this method to cancer etiology and prognosis, including Reverse Causation arising from disease latency and selection bias in studies of cancer progression. These issues must be carefully considered to ensure appropriate design, analysis, and interpretation of such studies. In this review, we provide an overview of the key principles and assumptions of MR, focusing on applications of this method to the study of cancer etiology and prognosis. We summarize recent studies in the cancer literature that have adopted a MR framework to highlight strengths of this approach compared with conventional epidemiological studies. Finally, limitations of MR and recent methodologic developments to address them are discussed, along with the translational opportunities they present to inform public health and clinical interventions in cancer. Cancer Epidemiol Biomarkers Prev; 27(9); 995-1010. ©2018 AACR.
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causal inference in cancer epidemiology what is the role of mendelian randomization
bioRxiv, 2017Co-Authors: James Yarmolinsky, George Davey Smith, Kaitlin H Wade, Caroline L Relton, Rebecca C Richmond, Ryan Langdon, Caroline J Bull, Kate Tilling, Sarah J Lewis, Richard M MartinAbstract:Observational epidemiological studies are prone to confounding, measurement error, and Reverse Causation, undermining their ability to generate reliable causal estimates of the effect of risk factors to inform cancer prevention and treatment strategies. Mendelian randomization (MR) is an analytical approach that uses genetic variants to proxy potentially modifiable exposures (e.g. environmental factors, biological traits, and druggable pathways) to permit robust causal inference of the effects of these exposures on diseases and their outcomes. MR has seen widespread adoption within population health research in cardio-metabolic disease, but also holds much promise for identifying possible interventions (e.g., dietary, behavioural, or pharmacological) for cancer prevention and treatment. However, some methodological and conceptual challenges in the implementation of MR are particularly pertinent when applying this method to cancer aetiology and prognosis, including Reverse Causation arising from disease latency and selection bias in studies of cancer progression. These issues must be carefully considered to ensure appropriate design, analysis, and interpretation of such studies. In this review, we provide an overview of the key principles and assumptions of MR focusing on applications of this method to the study of cancer aetiology and prognosis. We summarize recent studies in the cancer literature that have adopted a MR framework to highlight strengths of this approach compared to conventional epidemiological studies. Lastly, limitations of MR and recent methodological developments to address them are discussed, along with the translational opportunities they present to inform public health and clinical interventions in cancer.
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association between genetically elevated levels of inflammatory biomarkers and risk of schizophrenia a two sample mendelian randomisation study
bioRxiv, 2017Co-Authors: Fernando Pires Hartwig, Jack Bowden, Maria Carolina Borges, Bernardo L Horta, George Davey SmithAbstract:Background: Positive associations between inflammatory biomarkers and risk of psychiatric disorders, including schizophrenia, have been reported in observational studies. However, conventional observational studies are prone to bias such as Reverse Causation and residual confounding. Methods: In this study, we used summary data to evaluate the association of genetically elevated C reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra) and soluble interleukin-6 receptor (IL-6R) levels with schizophrenia in a two-sample Mendelian randomisation design. Results: The pooled odds ratio estimate using 18 CRP genetic instruments was 0.90 (95% CI: 0.84; 0.97) per two-fold increment in CRP levels; consistent results were obtained using different Mendelian randomisation methods and a more conservative set of instruments. The odds ratio for soluble IL-6R was 1.06 (95% CI: 1.01; 1.12) per two-fold increment. Estimates for IL-1Ra were inconsistent among instruments and pooled estimates were imprecise and centred on the null. Conclusion: Under Mendelian randomisation assumptions, our findings suggest a protective causal effect of CRP and a risk-increasing causal effect of soluble IL-6R (potentially mediated at least in part by CRP) on schizophrenia risk.
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abstract 817 mendelian randomization and mediation analysis of 5p15 33 telomere length and lung cancer risk
Cancer Research, 2016Co-Authors: Linda Kachuri, George Davey Smith, Geoffrey Liu, Maria Teresa Landi, David C Christiani, Neil E Caporaso, James Mckay, Melinda C Aldrich, Gad Rennert, Dawn TeareAbstract:Background: Telomere length (TL) is a predictor of lung cancer risk, but the direction of this association differs between and prospective and case-control studies. This discrepancy may be attributed to Reverse Causation in the latter, due to disease-related changes in TL that is measured after diagnosis or treatment. To overcome these limitations and characterize the relationship between TL and lung cancer risk we carried out observational and mediation analyses, and a 2-stage Mendelian Randomization (MR) analysis, where we developed novel genetic instruments for TL and tested the association with lung cancer using 20 OncoArray studies in the Transdisciplinary Research in Cancer of the Lung group of the International Lung Cancer Consortium. Methods: The observational analysis examined TL measured using qPCR in 1128 cases and 928 controls. Odds ratios (OR) for TL were adjusted for age, sex and cigarette pack-years. Mediation analysis was used to estimate the% of the lung cancer association in 5p15 that operates through TL. To develop novel TL instruments, variants identified through deep sequencing of the 5p15 locus were genotyped in 900 controls. Variants that met MR criteria were combined into a single instrumental variable (IV), and its association with TL was estimated. We also used 6 previously identified TL predictors (p Results: The observational analysis suggested that longer TL is associated with decreased lung cancer risk (OR = 0.94, p = 0.04). This was more pronounced for squamous carcinoma (OR = 0.77, p = 1.1×10-4). We also showed that TL mediates up to 8% (p Conclusions: We developed novel genetic instruments for TL, and confirmed that genetically predicted longer TL is associated with increased lung cancer risk. These findings suggest that previously reported associations of long TL with decreased risk were likely due to residual confounding by smoking, age and/or Reverse Causation. Citation Format: Linda Kachuri, George Davey Smith, Geoffrey Liu, Maria Teresa Landi, David C. Christiani, Neil E. Caporaso, James D. McKay, Xifeng Wu, Melinda C. Aldrich, Gad Rennert, Dawn Teare, Chu Chen, Gary E. Goodman, Jennifer A. Doherty, John K. Field, Lambertus A. Kiemeney, Adonina Tardon, Aage Haugen, Stephen Lam, Loic Le Marchand, Matthew B. Schabath, Angeline S. Andrew, Mattias Johansson, Jonas Manjer, Philip Lazarus, Susanne Arnold, Gordon Fehringer, Xuchen Zong, Paul Brennan, Stig E. Bojesen, Christopher I. Amos, Rayjean J. Hung. Mendelian randomization and mediation analysis of 5p15.33, telomere length and lung cancer risk. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 817.
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best but oft forgotten practices the design analysis and interpretation of mendelian randomization studies
The American Journal of Clinical Nutrition, 2016Co-Authors: Philip C Haycock, Stephen Burgess, Kaitlin H Wade, Jack Bowden, Caroline L Relton, George Davey SmithAbstract:Mendelian randomization (MR) is an increasingly important tool for appraising causality in observational epidemiology. The technique exploits the principle that genotypes are not generally susceptible to Reverse Causation bias and confounding, reflecting their fixed nature and Mendel’s first and second laws of inheritance. The approach is, however, subject to important limitations and assumptions that, if unaddressed or compounded by poor study design, can lead to erroneous conclusions. Nevertheless, the advent of 2-sample approaches (in which exposure and outcome are measured in separate samples) and the increasing availability of open-access data from large consortia of genome-wide association studies and population biobanks mean that the approach is likely to become routine practice in evidence synthesis and causal inference research. In this article we provide an overview of the design, analysis, and interpretation of MR studies, with a special emphasis on assumptions and limitations. We also consider different analytic strategies for strengthening causal inference. Although impossible to prove causality with any single approach, MR is a highly cost-effective strategy for prioritizing intervention targets for disease prevention and for strengthening the evidence base for public health policy.
Mika Kivimaki - One of the best experts on this subject based on the ideXlab platform.
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physical inactivity cardiometabolic disease and risk of dementia an individual participant meta analysis
BMJ, 2019Co-Authors: Archana Singhmanoux, Mika Kivimaki, Jaana Pentti, Severine Sabia, Solja T Nyberg, Lars AlfredssonAbstract:OBJECTIVE To examine whether physical inactivity is a risk factor for dementia, with attention to the role of cardiometabolic disease in this association and Reverse Causation bias that arises from ...
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body mass index and risk of dementia analysis of individual level data from 1 3 million individuals
Alzheimers & Dementia, 2018Co-Authors: Mika Kivimaki, Jaana Pentti, Ritva Luukkonen, David G Batty, Jane E Ferrie, Solja T NybergAbstract:Abstract Introduction Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects. Methods We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis. Results Hazard ratios per 5-kg/m 2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66–0.77), 0.94 (0.89–0.99), and 1.16 (1.05–1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis. Conclusions The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a Reverse-Causation effect that makes a higher BMI to appear protective when the follow-up is short.
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depressive disorder coronary heart disease and stroke dose response and Reverse Causation effects in the whitehall ii cohort study
European Journal of Preventive Cardiology, 2014Co-Authors: Eric J Brunner, Martin J Shipley, Annie Britton, Stephen Stansfeld, Peter U Heuschmann, Anthony Rudd, Charles D A Wolfe, Archana Singhmanoux, Mika KivimakiAbstract:BackgroundSystematic reviews examining associations of depressive disorder with coronary heart disease and stroke produce mixed results. Failure to consider Reverse Causation and dose–response patterns may have caused inconsistencies in evidence.DesignThis prospective cohort study on depressive disorder, coronary heart disease, and stroke analysed Reverse Causation and dose–response effects using four 5-year and three 10-year observation cycles (total follow up 24 years) based on multiple repeat measures of exposure.MethodsParticipants in the Whitehall II study (n = 10,036, 31,395 person-observations, age at start 44.4 years) provided up to six repeat measures of depressive symptoms via the 30-item General Health Questionnaire (GHQ-30) and one measure via Center for Epidemiologic Studies Depression Scale (CES-D). The cohort was followed up for major coronary events (coronary death/nonfatal myocardial infarction) and stroke (stroke death/morbidity) through the national mortality register Hospital Episode S...
Maarten Kroesen - One of the best experts on this subject based on the ideXlab platform.
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Residential self-selection and the Reverse Causation hypothesis: Assessing the endogeneity of stated reasons for residential choice
Travel Behaviour and Society, 2019Co-Authors: Maarten KroesenAbstract:Residential self-selection is a well-recognized potential bias in estimating the true effects of the built environment on travel behavior. A popular method to account for residential self-selection is by including people's attitudes towards various modes as additional control variables in the regression. Yet, while attitudes may indeed influence both residential location choice and travel behavior, they may, in turn, also be affected by these factors. This paper aims to assess to what extent the built environment and travel behavior influence people's stated reasons for living in a certain location over time, which would mean that these reasons are actually endogenous to the built environment and travel behavior. To achieve this aim panel data are used from the same respondents (who did not move house)asking them at two points in time (two years apart)to state their reasons for their current residential choice. The data are modeled using a latent transition model. The results indicate that approximately 39% of the Dutch population belongs to a class which attaches importance to short distances to public transport and shops. Moreover, the distance to the train station, the amount of travel by train and car ownership at the first point in time are found to influence the probability that a person (still)belongs to this class at the second point in time, providing evidence that the built environment and travel behavior temporally precede travel related residential preferences. The results suggest that the use of stated reasons for residential choice as control variables is problematic.
Anderson, Jana J. - One of the best experts on this subject based on the ideXlab platform.
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The associations of sugar-sweetened, artificially sweetened and naturally sweet juices with all-cause mortality in 198,285 UK Biobank participants: a prospective cohort study
BMC, 2020Co-Authors: Anderson, Jana J., Gray, Stuart R, Welsh Paul, Mackay, Daniel F., Celis-morales, Carlos A., Lyall, Donald M., Forbes, John F., Sattar Naveed, Gill, Jason M. R., Pell, Jill P.Abstract:Background: Recent efforts to address the obesity epidemic have focused on sugar consumption, especially sugar-sweetened beverages. However, sugar takes many forms, is only one contributor to overall energy consumption and is correlated with other health-related lifestyle factors. The objective was to investigate the associations with allcause mortality of sugar- and artificially sweetened beverages and naturally sweet juices. Methods: Setting: UK Biobank, UK. Participants joined the UK Biobank study from 2006 to 2010 and were followed up until 2016; 198,285 men and women aged 40–69 years were eligible for this study (40% of the UK Biobank), of whom 3166 (1.6%) died over a mean of 7 years follow-up. Design: prospective population-based cohort study. Exposure variables: dietary consumption of sugar-sweetened beverages, artificially sweetened beverages, naturally sweet juices (100% fruit/vegetable juices) and total sugar intake, self-reported via 24-h dietary assessment tool completed between 2009 and 2012. Main outcome: all-cause mortality. Cox regression analyses were used to study the association between the daily intake of the above beverages and all-cause mortality. Models were adjusted for socio-demographic, economic, lifestyle and dietary confounders. Results: Total energy intake, total sugar intake and percentage of energy derived from sugar were comparable among participants who consumed > 2/day sugar-sweetened beverages and > 2/day fruit/vegetable juices (10,221 kJ/day versus 10,381 kJ/day; 183 g versus 190 g; 30.6% versus 31.0%). All-cause mortality was associated with total sugar intake (highest quintile adj. HR 1.28, 95% CI 1.06–1.55) and intake of sugar-sweetened beverages (> 2/day adj. HR 1.84, 95% CI 1.42–2.37) and remained so in sensitivity analyses. An association between artificially sweetened beverage intake and mortality did not persist after excluding deaths in the first 2 years of follow-up (landmark analysis) nor after excluding participants with recent weight loss. Furthermore, the inverse association between fruit/vegetable juice intake and mortality did not persist after additional adjustment for a diet quality score. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation
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The associations of sugar-sweetened, artificially sweetened and naturally sweet juices with all-cause mortality in 198,285 UK Biobank participants: a prospective cohort study
'Springer Science and Business Media LLC', 2020Co-Authors: Anderson, Jana J., Gray, Stuart R, Welsh Paul, Mackay, Daniel F., Celis-morales, Carlos A., Lyall, Donald M., Forbes, John F., Sattar Naveed, Gill, Jason M. R., Pell, Jill P.Abstract:peer-reviewedBackground: Recent efforts to address the obesity epidemic have focused on sugar consumption, especially sugar-sweetened beverages. However, sugar takes many forms, is only one contributor to overall energy consumption and is correlated with other health-related lifestyle factors. The objective was to investigate the associations with allcause mortality of sugar- and artificially sweetened beverages and naturally sweet juices. Methods: Setting: UK Biobank, UK. Participants joined the UK Biobank study from 2006 to 2010 and were followed up until 2016; 198,285 men and women aged 40–69 years were eligible for this study (40% of the UK Biobank), of whom 3166 (1.6%) died over a mean of 7 years follow-up. Design: prospective population-based cohort study. Exposure variables: dietary consumption of sugar-sweetened beverages, artificially sweetened beverages, naturally sweet juices (100% fruit/vegetable juices) and total sugar intake, self-reported via 24-h dietary assessment tool completed between 2009 and 2012. Main outcome: all-cause mortality. Cox regression analyses were used to study the association between the daily intake of the above beverages and all-cause mortality. Models were adjusted for socio-demographic, economic, lifestyle and dietary confounders. Results: Total energy intake, total sugar intake and percentage of energy derived from sugar were comparable among participants who consumed > 2/day sugar-sweetened beverages and > 2/day fruit/vegetable juices (10,221 kJ/day versus 10,381 kJ/day; 183 g versus 190 g; 30.6% versus 31.0%). All-cause mortality was associated with total sugar intake (highest quintile adj. HR 1.28, 95% CI 1.06–1.55) and intake of sugar-sweetened beverages (> 2/day adj. HR 1.84, 95% CI 1.42–2.37) and remained so in sensitivity analyses. An association between artificially sweetened beverage intake and mortality did not persist after excluding deaths in the first 2 years of follow-up (landmark analysis) nor after excluding participants with recent weight loss. Furthermore, the inverse association between fruit/vegetable juice intake and mortality did not persist after additional adjustment for a diet quality score. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation. Conclusions: Higher mortality is associated with sugar-sweetened beverages specifically. The lack of an adverse association with fruit/vegetable juices suggests that source of sugar may be important and the association with artificially sweetened beverage may reflect Reverse Causation
