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Genetically high plasma vitamin C and urate: a Mendelian randomization study in 106 147 individuals from the general population.
- Source :
-
Rheumatology . Oct2018, Vol. 57 Issue 10, p1769-1776. 8p. 1 Diagram, 2 Charts, 2 Graphs. - Publication Year :
- 2018
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Abstract
- Objective Gout is the most common form of inflammatory arthritis and is caused by hyperuricaemia. Some studies have found a reduction in plasma urate with vitamin C supplementation. We tested the hypothesis that high plasma vitamin C is causally associated with low plasma urate and low risk of hyperuricaemia, using a Mendelian randomization approach. Methods We measured plasma urate and genotyped for the SLC23A1 rs33972313 vitamin C variant in 106 147 individuals from the Copenhagen General Population Study, of which 24 099 had hyperuricaemia. We measured plasma vitamin C in 9234 individuals and genotyped for the SLC2A9 rs7442295 urate variant in 102 345 individuals. Results Each 10 µmol/l higher plasma vitamin C was associated with a −2.3(95%CI: −0.69 to −3.9) µmol/l lower plasma urate after multivariable adjustments. The SLC23A1 rs33972313 GG genotype was associated with a 9% (5.6%, 11.9%) higher plasma vitamin C compared with AA and AG combined but was not associated with plasma urate (P = 0.31). Likewise, for each 10 µmol/l higher plasma vitamin C the odds ratios for hyperuricaemia were 0.92 (0.86, 0.98) observationally after multivariable adjustments, but 1.01 (0.84, 1.23) genetically. Conclusion High plasma vitamin C was associated with low plasma urate and with low risk of hyperuricaemia. However, the SLC23A1 genetic variant causing lifelong high plasma vitamin C was not associated with plasma urate levels or with risk of hyperuricaemia. Thus, our data do not support a causal relationship between high plasma vitamin C and low plasma urate. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 14620324
- Volume :
- 57
- Issue :
- 10
- Database :
- Academic Search Index
- Journal :
- Rheumatology
- Publication Type :
- Academic Journal
- Accession number :
- 131968909
- Full Text :
- https://doi.org/10.1093/rheumatology/key171