A variant in CYP2R1 predicts circulating vitamin D levels after supplementation with high-dose of vitamin D in healthy adolescent girls
J Cell Physiol. 2019 Aug;234(8):13977-13983. doi: 10.1002/jcp.28083
- CYP2R1 gene reduces response to Vitamin D - many studies
- On-line Vitamin D response simulation – July 2021
Genetics category listing contains the following
see also
- Vitamin D Receptor has
530 items - Vitamin D Binding Protein = GC has
177 items - CYP27B1 has
63 items - CYP24A1 in title of 34+ items
- CYP2R1 25+ items
- Calcidiol has
48 items - Calcitriol has
62 items - Topical Vitamin D
- Nanoemulsion Vitamin D may be a substantially better form
- 1289 genes changed with higher doses of Vitamin D - RCT Dec 2019
- CYP3A4 (7 as of Dec 2022)
- Getting Vitamin D into your body
Vitamin D blood test misses a lot
- Vitamin D from coming from tissues (vs blood) was speculated to be 50% in 2014, and by 2017 was speculated to be 90%
- Note: Good blood test results (> 40 ng) does not mean that a good amount of Vitamin D actually gets to cells
- A Vitamin D test in cells rather than blood was feasible (2017 personal communication) Commercially available 2019
- However, test results would vary in each tissue due to multiple genes
- Good clues that Vitamin D is being restricted from getting to the cells
1) A vitamin D-related health problem runs in the family
especially if it is one of 51+ diseases related to Vitamin D Receptor
2) Slightly increasing Vitamin D shows benefits (even if conventional Vitamin D test shows an increase)
3) DNA and VDR tests - 120 to 200 dollars $100 to $250
4) PTH bottoms out ( shows that parathyroid cells are getting Vitamin d)
Genes are good, have enough Magnesium, etc.
5) Back Pain
probably want at least 2 clues before taking adding vitamin D, Omega-3, Magnesium, Resveratrol, etc- The founder of VitaminDWiki took action with clues #3&5
Download the PDF from VitaminDWiki
Aim: The determinants of serum vitamin D seems to be the environmental factors (dietary and supplementary intake and exposure to ultraviolet light) and genetic factors. We aimed to study the relationship between a vitamin D-associated genetic polymorphism and serum 25(OH)D concentrations in healthy adolescent girls in Iran, and its effects on a high-dose supplement of vitamin D.
Material and method: A total of 616 healthy adolescent girls with mean age 15 received 50,000 IU of vitamin D3 weekly over 9 weeks. Serum vitamin D levels and other metabolic factors were measured at baseline and after the intervention. The genotyping of the CYP2R1 variant (rs10741657) was performed by TaqMan genotyping assays.
Results: Regardless of the genetic background, at baseline, 87% of adolescent girls were vitamin D deficient (serum 25(OH)D level < 50 nmol/l). High-dose supplementation with VitD reduced the proportion of girls who were deficient substantially to about 24%. The genetic analysis revealed that although at baseline there was not a gene-vitamin D association (p trend = 0.1), the response to supplementation appeared to be modulated by this variant (p trend < 0.001). However, other anthropometric and biochemical measures were not affected by this intervention, over this short period. Serum 25(OH)D was increased in all participants although the carriers of the minor A allele seemed to be better responders so that the percentages of the change serum vitamin D in the holder of AA and AG genotypes were 539.4 ±443.1 and 443.7 ±384.6, respectively, compared with those with common GG genotype (363.3 ± 354.0). Our regression analysis revealed that the probability of an increase in serum 25(OH)D in a participant with AA genotype was 2.5-fold greater than those with a GG genotype (OR = 2.5 (1.4-4.4); p value = 0.002).
Conclusion: Based on our findings, it appears that the rs10741657 variant of the CYP2R1 gene modulates the response to high-dose of vitamin D supplementation.
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