Evidence of a Causal Link Between the Well-Being Spectrum and the Risk of Myocardial Infarction: A Mendelian Randomization Study
[ABSTRACT READ IN FULL AT SOURCE, the Frontiers full-text page, open access; THE BODY WAS READ ONLY IN PART, covering the instrument description and the pleiotropy checks] Rukh, G., Ahmad, S., Lind, L., & Schioth, H. B. (2022). 'Evidence of a Causal Link Between the Well-Being Spectrum and the Risk of Myocardial Infarction: A Mendelian Randomization Study.' Frontiers in Genetics 13, 842223. doi:10.3389/fgene.2022.842223. THE POSITIVE MENDELIAN RANDOMISATION RESULT, AND IT IS A COMPOSITE. The instrument is 231 independent single-nucleotide polymorphisms for a wellbeing spectrum derived from FOUR traits: life satisfaction, positive affect, neuroticism and depressive symptoms. Four outcomes: atrial fibrillation, heart failure, myocardial infarction and ischaemic stroke. Result, verbatim: 'The genetically predicted WBS was associated with 38% lower risk for heart failure (odds ratio (OR): 0.62; 95% CI: 0.50-0.78) and 40% reduced risk of myocardial infarction (OR: 0.60; 95% CI: 0.47-0.78). Of the WBS constituent traits, only depressive symptoms showed a positive causal association with heart failure and myocardial infarction. Neither WBS nor WBS constituent traits were associated with atrial fibrillation and ischemic stroke ... the association is mainly driven by depressive symptoms.' The MR-Egger intercept showed no evidence of directional pleiotropy; in multivariable analysis accounting for traditional risk factors the estimates attenuated to 0.72 for heart failure and 0.67 for myocardial infarction. The reconciliation with the 2018 null is the article's argument: wellbeing alone gives no causal effect, a composite containing depressive symptoms gives one that its own authors attribute to the depressive symptoms. NEITHER STUDY MEASURED DISPOSITIONAL OPTIMISM.
[ABSTRACT READ IN FULL AT SOURCE, the Frontiers full-text page, open access; THE BODY WAS READ ONLY IN PART, covering the instrument description and the pleiotropy checks] Rukh, G., Ahmad, S., Lind, L., & Schioth, H. B. (2022). 'Evidence of a Causal Link Between the Well-Being Spectrum and the Risk of Myocardial Infarction: A Mendelian Randomization Study.' Frontiers in Genetics 13, 842223. doi:10.3389/fgene.2022.842223. THE POSITIVE MENDELIAN RANDOMISATION RESULT, AND IT IS A COMPOSITE. The instrument is 231 independent single-nucleotide polymorphisms for a wellbeing spectrum derived from FOUR traits: life satisfaction, positive affect, neuroticism and depressive symptoms. Four outcomes: atrial fibrillation, heart failure, myocardial infarction and ischaemic stroke. Result, verbatim: 'The genetically predicted WBS was associated with 38% lower risk for heart failure (odds ratio (OR): 0.62; 95% CI: 0.50-0.78) and 40% reduced risk of myocardial infarction (OR: 0.60; 95% CI: 0.47-0.78). Of the WBS constituent traits, only depressive symptoms showed a positive causal association with heart failure and myocardial infarction. Neither WBS nor WBS constituent traits were associated with atrial fibrillation and ischemic stroke ... the association is mainly driven by depressive symptoms.' The MR-Egger intercept showed no evidence of directional pleiotropy; in multivariable analysis accounting for traditional risk factors the estimates attenuated to 0.72 for heart failure and 0.67 for myocardial infarction. The reconciliation with the 2018 null is the article's argument: wellbeing alone gives no causal effect, a composite containing depressive symptoms gives one that its own authors attribute to the depressive symptoms. NEITHER STUDY MEASURED DISPOSITIONAL OPTIMISM.
Written from the aBSTRACT READ IN FULL AT SOURCE, the Frontiers full-text page, open access; THE BODY WAS READ ONLY IN PART, covering the instrument description and the pleiotropy checks.
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Rukh, G., Ahmad, S., Lind, L., & Schioth, H. B. (2022). Evidence of a Causal Link Between the Well-Being Spectrum and the Risk of Myocardial Infarction: A Mendelian Randomization Study. Frontiers in Genetics, 13, 842223. doi:10.3389/fgene.2022.842223