TABLE 2.
Exposure | Outcome | n SNPs | IVW | Weighted Median | Weighted Mode | MR‐Egger |
n SNPs a |
GSMR | |||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
β | OR | 95% CI | P | β | OR | 95% CI | P | β | OR | 95% CI | P | β | OR | 95% CI | P | β | OR | 95% CI | P | ||||
Smoking initiation | ADHD | 346 | 1.31 | 3.72 | 3.10 to 4.44 | 2.9e−51 | 1.18 | 3.26 | 2.59 to 4.14 | 5.0e−22 | 1.04 | 2.84 | 1.17 to 6.82 | .021 | 1.00 | 2.72 | 1.48 to 5.00 | .001 | 330 | 1.24 | 3.46 | 2.89 to 4.14 | 1.4e−44 |
Alcohol drinks/wk | ADHD | 90 | 0.01 | 1.01 | 0.57 to 1.79 | .975 | 0.01 | 1.01 | 0.44 to 2.34 | .978 | −0.17 | 0.84 | 0.29 to 2.44 | .747 | −0.46 | 0.63 | 0.19 to 2.10 | .444 | 80 | 1.08 | 2.95 | 1.67 to 5.21 | .788 |
Alcohol problems | ADHD | 7 | 0.59 | 1.81 | 0.14 to 24.05 | .655 | 0.52 | 1.68 | 0.07 to 41.68 | .752 | 0.78 | 2.18 | 0.03 to 165.67 | .736 | n.a. | n.a. | n.a. | n.a. | 7 | n.a. | n.a. | n.a. | n.a. |
Alcoholdependence | ADHD | 9 | −0.23 | 0.80 | 0.53 to 1.20 | .283 | −0.13 | 0.88 | 0.52 to 1.49 | .633 | −0.69 | 0.50 | 0.21 to 1.21 | .162 | n.a. | n.a. | n.a. | n.a. | 9 | n.a. | n.a. | n.a. | n.a. |
Cannabis initiation | ADHD | 5 | 0.38 | 1.46 | 0.93 to 2.29 | .103 | 0.48 | 1.62 | 1.01 to 2.59 | .044 | 0.57 | 1.77 | 0.98 to3.19 | .132 | n.a. | n.a. | n.a. | n.a. | 5 | n.a. | n.a. | n.a. | n.a. |
Coffee/d | ADHD | 4 | −0.01 | 0.99 | 0.66 to 1.49 | .969 | −0.01 | 0.99 | 0.73 to 1.35 | .923 | 0.01 | 1.01 | 0.70 to1.46 | .951 | n.a. | n.a. | n.a. | n.a. | 4 | n.a. | n.a. | n.a. | n.a. |
Note. The dichotomous variable smoking initiation was rescaled in the original GWAS such that its unit is a standard deviation increase in prevalence. 17 The ORs in this table reflect the change in ADHD diagnosis odds for a one‐unit increase in the exposure variable in the case of continuous exposure variables and the change in ADHD diagnosis odds per 2.72‐fold increase in the prevalence of the exposure variable for binary exposure variables (due to the log odds nature of the binary exposure GWAS data). For MR‐Egger, when I 2 was 0.6‐0.9, a SIMEX correction was applied, while estimates were not reported at all when I 2 was <0.6.
ADHD, attention‐deficit hyperactivity disorder; GSMR, generalized summary‐level‐data based Mendelian randomization; GWAS, genome‐wide association studies; n SNPs, number of SNPs included in the genetic instrument; n.a., the number of SNPs available for the analysis was too low, or, in the case of MR‐Egger, I 2 was <0.6; SE, standard error of the beta; SIMEX, simulation extrapolation.
Number of SNPs left after the HEIDI filtering step, which is part of GSMR.