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Items: 5

1.
Figure 1b

Figure 1b. Association of WHRadjBMI with continuous biomarkers derived from Mendelian randomization analysis.. From: Causal Associations of Adiposity and Body Fat Distribution with Coronary Heart Disease, Stroke Subtypes and Type 2 Diabetes: A Mendelian Randomization Analysis.

Values represent standardized mean differences of each trait per SD increase in WHRadjBMI derived from conventional (IVW) Mendelian randomization analysis. Non-normally distributed variables were natural log transformed; therefore mean differences displayed on the log scale may be anti-logged and interpreted as percentage difference in SD of trait per SD in WHRadjBMI. Log triglycerides from individual participant data studies only; GLGC triglycerides in .

Caroline E. Dale, et al. Circulation. ;135(24):2373-2388.
2.
Figure 1a

Figure 1a. Association of BMI with continuous biomarkers derived from Mendelian randomization analysis.. From: Causal Associations of Adiposity and Body Fat Distribution with Coronary Heart Disease, Stroke Subtypes and Type 2 Diabetes: A Mendelian Randomization Analysis.

Values represent standardized mean differences of each trait per SD increase in BMI derived from conventional (IVW) Mendelian randomization analysis. Non-normally distributed variables were natural ln transformed; therefore mean differences displayed on the log scale may be anti-logged and interpreted as percentage differences in SD of trait per SD in BMI. Log triglycerides from individual participant data studies only; GLGC triglycerides in .

Caroline E. Dale, et al. Circulation. ;135(24):2373-2388.
3.
Figure 2c

Figure 2c. Associations of adiposity with risk of T2D from observational and Mendelian randomization analyses.. From: Causal Associations of Adiposity and Body Fat Distribution with Coronary Heart Disease, Stroke Subtypes and Type 2 Diabetes: A Mendelian Randomization Analysis.

Association between T2D and adiposity (BMI and WHRadjBMI) comparing causal odds ratios (OR) per SD of adiposity trait derived from instrumental variable analysis and observational analysis from Vazquez et al., 2007. Causal estimates are derived from Mendelian randomization and include conventional (ratio) approach and weighted median (see for further details). P(genetic pleiotropy) relates to the P-value derived from the intercept of MR-Egger; a small P-value denotes presence of directional pleiotropy.

Caroline E. Dale, et al. Circulation. ;135(24):2373-2388.
4.
Figure 2b

Figure 2b. Associations of adiposity with risk of ischaemic stroke from observational and Mendelian randomization analyses.. From: Causal Associations of Adiposity and Body Fat Distribution with Coronary Heart Disease, Stroke Subtypes and Type 2 Diabetes: A Mendelian Randomization Analysis.

Association between ischaemic stroke and adiposity (BMI and WHRadjBMI) comparing causal odds ratios (OR) per SD of adiposity trait derived from instrumental variable analysis and observational analysis from the Emerging Risk Factors Consortium (HR of ischaemic stroke per SD of BMI or waist:hip adjusted for age, sex and smoking status). Causal estimates are derived from Mendelian randomization and include conventional (ratio) approach and weighted median (see for further details). P(genetic pleiotropy) relates to the P-value derived from the intercept of MR-Egger; a small P-value denotes presence of directional pleiotropy.

Caroline E. Dale, et al. Circulation. ;135(24):2373-2388.
5.
Figure 2a

Figure 2a. Associations of adiposity with risk of CHD from observational and Mendelian randomization analyses.. From: Causal Associations of Adiposity and Body Fat Distribution with Coronary Heart Disease, Stroke Subtypes and Type 2 Diabetes: A Mendelian Randomization Analysis.

Association between coronary heart disease and adiposity (BMI and WHRadjBMI) comparing causal odds ratios (OR) per SD of adiposity trait derived from instrumental variable analysis and observational analysis from the Emerging Risk Factors Consortium hazard ratio (HR per SD of BMI or waist:hip adjusted for age, sex and smoking status). Causal estimates are derived from Mendelian randomization and include conventional (ratio) approach and weighted median (see for further details). P(genetic pleiotropy) relates to the P-value derived from the intercept of MR-Egger; a small P-value denotes presence of directional pleiotropy.

Caroline E. Dale, et al. Circulation. ;135(24):2373-2388.

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