A GC polymorphism associated with serum 25-hydroxyvitamin D level is a risk factor for hip fracture in Japanese patients with rheumatoid arthritis: 10-year follow-up of the Institute of Rheumatology, Rheumatoid Arthritis cohort study.
Arthritis Res Ther. 2014 Mar 20;16(2):R75. doi: 10.1186/ar4516.
Yoshida S, Ikari K, Furuya T, Toyama Y, Taniguchi A, Yamanaka H, Momohara S.
GC results in only a small reduction in MEASURED levels of vitamin D
But probably large reduction in the free/bioavailable vitamin D which actually gets to the cells. which is not measured
See also VitaminDWiki
- Genes make Multiple Sclerosis 2X more likely unless get more vitamin D - Aug 2015
- Gene makes COPD 2.6X more likely unless get more vitamin D – meta-analysis Dec 2014
GC and 3 other Genes
- Vitamin D and fractures – 24 meta-analyses and counting – Dec 2014
- Bone fractures reduced by a minimum of 800 IU vitamin D and Calcium – meta-meta-analysis March 2014
- GC gene 365 hits as of Aug 2015
- Overview Fractures and vitamin D
- Genes (CYP2R1 and GC) which restrict the amount of Vitamin D which gets into bloodstream – June 2014
- All items in category Vitamin D Binding Protein (affected by GC)
- Bioavailable Vitamin D is the same blacks and whites, but measured vit D is not – Oct 2014
- Genes are one of the reasons for low response to vitamin D – Nov 2014
- Gene makes COPD 2.6X more likely unless get more vitamin D – meta-analysis Dec 2014 similar to study on this page
- Vitamin D tests assume constant Binding Protein - not correct across races and clinical situations – July 2014
- Testing misses the Vitamin D tied up with VDBP – June 2014
- 68+ pages with hip tracture in title as of Dec 2022
GC makes a small reduction in MEASURED level of Vitamin D
But perhaps a large reduction in the FREE vitamin D which actually gets to the cells
INTRODUCTION: Vitamin D deficiency has been reported to be common in patients with rheumatoid arthritis (RA) who have a higher prevalence of osteoporosis and hip fracture than healthy individuals. Genetic variants affecting serum 25-hydroxyvitamin D (25(OH)D) concentration, an indicator of vitamin D status, were recently identified by genome-wide association studies of Caucasian populations. The purpose of this study was to validate the association and to test whether the serum 25(OH)D-linked genetic variants were associated with the occurrence of hip fracture in Japanese RA patients.
METHODS: DNA samples of 1,957 Japanese RA patients were obtained from the Institute of Rheumatology, Rheumatoid Arthritis (IORRA) cohort DNA collection. First, five single nucleotide polymorphisms (SNPs) that were reported to be associated with serum 25(OH)D concentration by genome-wide association studies were genotyped. The SNPs that showed a significant association with serum 25(OH)D level in the cross-sectional study were used in the longitudinal analysis of hip fracture risk. The genetic risk for hip fracture was determined by a multivariate Cox proportional hazards model in 1,957 patients with a maximum follow-up of 10 years (median, 8 years).
RESULTS: Multivariate linear regression analyses showed that rs2282679 in GC (the gene encoding group-specific component (vitamin D binding protein)) locus was significantly associated with lower serum 25(OH)D concentration (P = 8.1 × 10⁻⁵). A Cox proportional hazards model indicated that rs2282679 in GC was significantly associated with the occurrence of hip fracture in a recessive model (hazard ratio (95% confidence interval) = 2.52 (1.05-6.05), P = 0.039).
CONCLUSIONS: A two-staged analysis demonstrated that rs2282679 in GC was associated with serum 25(OH)D concentration and could be a risk factor for hip fracture in Japanese RA patients