Table 4. rs2282679 polymorphism association with diseases and traits that have been observationally related to vitamin D levels.
| CaMos Results | GWAS Meta-Analysis Results | ||||||
| Phenotype | CaMos Effect Estimate∫ | p-Value | Sample Size | GWAS Effect Estimate∫ | p-Value | Sample Size (Cases/Controls) | Consortium |
| Disease-related trait | |||||||
| 25OHD—nmol/l | −4.48 (−6.00, −2.97) | 7.3×10−9 | 2,254 | — | 1.9×10−109 | 33,996 | SUNLIGHT |
| Free 25OHD—pmol/l | −0.06 (−0.27, 0.39) | 0.72 | 2,254 | — | — | — | No consortium available |
| Calcium—mmol/l | −0.005 (−0.012, 0.001) | 0.12 | 2,250 | — | — | — | No consortium available |
| PTH∥—ng/l | −0.01 (−0.04, 0.01) | 0.34 | 2,083 | — | — | — | No consortium available |
| Fasting glucose—mmol/l | 0.01 (−0.05, 0.07) | 0.73 | 2,249 | 0.00 (−0.01, 0.01) | 0.997 | 46,186 | MAGIC |
| Fasting insulin∥—pmol/l | −0.03 (−0.07, 0.01) | 0.11 | 2,178 | −0.01 (−0.01, 0.003) | 0.22 | 46,186 | MAGIC |
| BMI—kg/m2 | −0.08 (−0.39, 0.23) | 0.63 | 2,167 | 0.00 (−0.01, 0.01) | 0.80 | 127,587 | GIANT |
| BMD at femoral neck—g/cm2 | 0.003 (−0.004, 0.01) | 0.43 | 2,213 | 0.01 (−0.01, 0.03) | 0.36 | 32,961 | GEFOS |
| Mean arterial pressure—mm Hg | — | — | — | −0.06 (−0.19, 0.07) | 0.36 | 28,775 | ICBP |
| Disease | |||||||
| Stroke/TIA | 1.45 (1.14, 1.85) | 0.003 | 2,122 | 1.00 (0.97, 1.04)| | 0.92 | 12,389/62,004 | METASTROKE/ISGC |
| Coronary artery disease | 1.13 (0.90, 1.42) | 0.30 | 2,122 | 1.02 (0.99, 1.05) | 0.31 | 22,233/64,762 | CARIDoGRAM |
| Diabetes | 0.99 (0.79, 1.24) | 0.93 | 2,122 | 1.01 (0.97, 1.05) | 0.76 | 9,580/53,810 | DIAGRAM |
| Hypertension | 1.12 (0.98, 1.28) | 0.11 | 2,116 | — | — | — | ICBP |
Regression models were adjusted for age and sex. Analyses of disease-related traits were performed on both adult and youth CaMos cohorts; analyses of diseases were restricted to the CaMos adult cohort only. M-dashes indicate that summary data were not publically available.
Measurement change for disease-related traits and OR for diseases. Change in measurement of disease-related trait is per each additional copy of the risk allele. All continuous variables were inspected for normality, and outliers (<1% of data points) were excluded. For diseases, ORs are reported per copy of risk allele. The null hypothesis is tested using α = 0.05. The Bonferroni method is used to maintain family-wise error rate when performing multiple testing through enforcing a more stringent α = 0.05/12 = 0.0042 (12 comparisons). Independence between outcomes was assumed in this correction.
The natural logarithm was used.
Effect estimates excluding participants with diabetes were similar for fasting glucose, −0.013 (95% CI −0.050, 0.023), p = 0.47, and for fasting insulin, −0.034 (95% CI −0.075, 0.007), p = 0.10.
ICBP had available GWAS data only on blood pressure measurements, not on hypertension; no association was found for systolic blood pressure, diastolic blood pressure, mean arterial pressure, and pulse pressure.
This effect estimate provided by METASTROKE is for overall ischemic stroke, which does not include TIA.