Table 1. Mendelian Randomization of Birth Weight and Risk of Type 2 Diabetes.
MR Estimatesa | Summary Data Ab | Summary Data Bb | ||
---|---|---|---|---|
OR (95% CI) | P Value | OR (95% CI) | P Value | |
Simple median–based methodc | 1.57(1.24 to 2.00) | 2.0 × 10-4 | 1.24(1.09 to 1.41) | .001 |
Weighted median–based methodc | 1.52(1.24 to 1.86) | 1.1 × 10-4 | 1.29(1.13 to 1.47) | 6.0 × 10-4 |
Inverse-variance–weighted methodc | 1.69(1.12 to 2.55) | .045 | 1.36(1.14 to 1.62) | .001 |
MR-Egger methodc | 2.79(1.90 to 4.20) | .02 | 1.96(1.07 to 3.60) | .03 |
MR-Egger regressiond | 0.007 (−0.081 to 0.095) | .94 | 0.011 (−0.002 to 0.02) | .22 |
Abbreviations: MR, mendelian randomization; OR, odds ratio.
In an MR framework, genetic variants for birth weight were assumed to influence type 2 diabetes only through birth weight, not through other pathways. In the present study, we used MR-Egger regression to assess for the presence of pleiotropy.16 This approach is based on Egger regression, which was used to assess publication bias in the meta-analysis.34 Using the MR-Egger method, the β coefficient of the MR-Egger regression provides pleiotropy-corrected causal estimates and an intercept distinct from the origin provides evidence for pleiotropic effects.16
Sample sizes of patients with type 2 diabetes and control individuals were 12 171 and 56 862 for both summary data A and summary data B. Number of single-nucleotide polymorphisms used of summary data A and summary data B are 7 and 43, respectively. Number of participants with birth weight in summary data A and summary data B are 69 308 and 153 781, respectively.
We used simple median–based method, weighted median–based method, inverse-variance–weighted method, and MR-Egger method to provide consistent results for causal effect of birth weight on type 2 diabetes.
Values in this row are intercept (95% CI).