Modifiable lifestyle factors and heart failure: A Mendelian randomization study

Oort, Sabine van; Beulens, Joline W.J.; Ballegooijen, Adriana J. van; Handoko, M. Louis; Larsson, Susanna C.

doi:10.1016/j.ahj.2020.06.007

Cited by 46 publications

(32 citation statements)

References 35 publications

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“…Our MR findings of no harmful effect of coffee consumption on cardiovascular disease risk corroborate and extend the results of traditional observational studies and previous MR studies of coffee consumption and risk of coronary artery disease [ 4 , 6 , 12 , 15 ], heart failure [ 8 , 14 ], atrial fibrillation [ 13 , 32 , 33 ], ischemic [ 11 ] and total stroke [ 7 ] as well as a phenome-wide study in the UK Biobank [ 34 ]. However, several observational studies have found that moderate coffee consumption (1–5 cups/day), but not heavy coffee consumption, is associated with a reduced risk of coronary artery disease [ 4 , 6 ], heart failure [ 8 ], atrial fibrillation [ 35 , 36 ] and total stroke [ 4 , 7 ].…”

Section: Discussionsupporting

confidence: 89%

“…The Mendelian randomization (MR) design [ 9 ] can improve causal inference by applying genetic variants as instrumental variables (proxies) for an exposure (e.g., coffee consumption) [ 10 ]. Results of recent MR studies found limited data in support of a causal association of coffee consumption with stroke [ 11 , 12 ], atrial fibrillation [ 13 ] and heart failure [ 14 ] but inconsistent findings for coronary artery disease [ 12 , 15 , 16 ]. Data are limited for associations of genetically predicted coffee consumption in relation to other cardiovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

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Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study

et al. 2021

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Coffee consumption has been linked to a lower risk of cardiovascular disease in observational studies, but whether the associations are causal is not known. We conducted a Mendelian randomization investigation to assess the potential causal role of coffee consumption in cardiovascular disease. Twelve independent genetic variants were used to proxy coffee consumption. Summary-level data for the relations between the 12 genetic variants and cardiovascular diseases were taken from the UK Biobank with up to 35,979 cases and the FinnGen consortium with up to 17,325 cases. Genetic predisposition to higher coffee consumption was not associated with any of the 15 studied cardiovascular outcomes in univariable MR analysis. The odds ratio per 50% increase in genetically predicted coffee consumption ranged from 0.97 (95% confidence interval (CI), 0.63, 1.50) for intracerebral hemorrhage to 1.26 (95% CI, 1.00, 1.58) for deep vein thrombosis in the UK Biobank and from 0.86 (95% CI, 0.50, 1.49) for subarachnoid hemorrhage to 1.34 (95% CI, 0.81, 2.22) for intracerebral hemorrhage in FinnGen. The null findings remained in multivariable Mendelian randomization analyses adjusted for genetically predicted body mass index and smoking initiation, except for a suggestive positive association for intracerebral hemorrhage (odds ratio 1.91; 95% CI, 1.03, 3.54) in FinnGen. This Mendelian randomization study showed limited evidence that coffee consumption affects the risk of developing cardiovascular disease, suggesting that previous observational studies may have been confounded.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study

et al. 2021

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“…Likewise, studies have shown a high heritability also for susceptibility to disease and longevity [78][79][80]. The lack of established causality between physical activity and CVD is further shown by mendelian randomization (MR) studies that have not been able to establish an association between genetically predicted accelerometermeasured physical activity and the risk of heart failure, coronary heart disease, myocardial infarction, and stroke [81,82]. Another MR study found that whereas genetic predisposition to a variety of metabolic risk factors and smoking were associated with lower odds of longevity, there was no such association for genetically predicted self-reported physical activity [83].…”

Section: Does Exercise Prevent Fractures In Older Adults?mentioning

confidence: 99%

Does exercise prevent major non‐communicable diseases and premature mortality? A critical review based on results from randomized controlled trials

Ballin

2021

J Intern Med

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“…This approach takes advantage of the naturally occurring random allocation of alleles at conception ( 18 ). Therefore, the level of a specific exposure will usually be independent of other exposures and unaffected by disease status ( 19 ). Thus, Mendelian randomization (MR) is capable of overcoming the limitations of residual confounding and reverse causation in observational studies.…”

Section: Introductionmentioning

confidence: 99%

Genetically Determined Inflammatory Biomarkers and the Risk of Heart Failure: A Mendelian Randomization Study

Peng

Guan

et al. 2021

Front. Cardiovasc. Med.

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Background: Positive associations between inflammatory biomarkers and the risk of heart failure (HF) have been reported in conventional observational studies. However, the causal effects of inflammatory biomarkers on HF have not been fully elucidated. We conducted a Mendelian randomization (MR) study to examine the possible etiological roles of inflammatory biomarkers in HF.Methods: Summary statistical data for the associations between single nucleotide polymorphisms (SNPs) and C-reactive protein (CRP), fibrinogen, and components of the interleukin-1 (IL-1)-interleukin-6 (IL-6) inflammatory signaling pathway, namely, interleukin-1β (IL-1β), IL-1 receptor antagonist (IL-1ra), IL-6, and soluble IL-6 receptor (sIL-6r), were obtained from genome-wide association studies (GWASs) for individuals of European descent. The GWAS dataset of 977,323 participants of European ancestry, which included 47,309 HF cases and 930,014 controls, was collected to identify genetic variants underlying HF. A two-sample Mendelian randomization framework was implemented to examine the causality of the association between these inflammatory biomarkers and HF.Results: Our MR analyses found that genetically determined CRP and fibrinogen were not causally associated with HF risk (odds ratio [OR] = 0.93, 95% confidence interval [CI] = 0.84–1.02, p = 0.15; OR = 0.94, 95% CI = 0.55–1.58, p = 0.80, respectively). These findings remained consistent using different Mendelian randomization methods and in sensitivity analyses. For the IL-1-IL-6 pathway, causal estimates for IL-6 (OR = 0.86, 95% CI 0.81–0.91, p < 0.001), but not for IL-1β, IL-1ra, or sIL-6r, were significant. However, the association between genetically determined IL-6 and HF risk became non-significant after excluding SNPs with potential pleiotropy (OR = 0.89, 95% CI = 0.77–1.03, p = 0.12).Conclusion: Our study did not identify convincing evidence to support that CRP and fibrinogen, together with their upstream IL-1-IL-6 signaling pathway, were causally associated with HF risk.

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Modifiable lifestyle factors and heart failure: A Mendelian randomization study

Cited by 46 publications

References 35 publications

Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study

Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study

Does exercise prevent major non‐communicable diseases and premature mortality? A critical review based on results from randomized controlled trials

Genetically Determined Inflammatory Biomarkers and the Risk of Heart Failure: A Mendelian Randomization Study

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