Bone. 2018 Oct 11. pii: S8756-3282(18)30370-3. doi: 10.1016/j.bone.2018.10.006. [Epub ahead of print]
This study appears to only look at the effect of genes on Vitamin D level in blood.
Seems to be unaware that genes can reduce the Vitamin D level in cells
Wonder if they consider the gene ACTIVATION effects on Vitamin D in cells
- Multiple Sclerosis risk increased due to genes - 22nd study – Aug 2017
- Afib increase by 3X for the 1 in 16 people having poor genes (example of health problem) – Aug 2018
- Health problems can persist through many generations – Epigenetics and Vitamin D
Genetics category listing contains the following
Vitamin D blood test misses a lot
- Snapshot of the literature by VitaminDWiki - (subject to many future developments)
- Vitamin D from coming from tissues (vs blood) was speculated to be 50% in 2014, andi in 2017 is speculated to be 90%
- Note: Good results from a blood test (> 40 ng) does not mean that a good amount of Vitamin D actually gets to cells
- A Vitamin D test in cells appears feasible (personal communication)
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 show benefits (even if conventional Vitamin D test shows an increase)
3) Vitamin D Receptor test (<$30) scores are difficult to understand in 2016
easier to understand the VDR 23andMe test results analyzed by FoundMyFitness in 2018
4) 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&4
PDF is available free at Sci-Hub 10.1016/j.bone.2018.10.006
Jiang X1, Kiel DP2, Kraft P3.
- 1 Program in Genetic Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Brookline, Boston 02115, USA; Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Nobels vagen 13, Stockholm 17177, Sweden xiajiang at hsph.harvard.edu.
- 2 Institute for Aging Research, Hebrew SeniorLife, 1200 Centre Street, Boston, MA 02131, United States; Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, United States; Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, MA 02142, United States.
- 3 Program in Genetic Epidemiology, Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Brookline, Boston 02115, USA.
Vitamin D plays an essential role in human health as it influences immune function, cell proliferation, differentiation and apoptosis. Vitamin D deficiency has been associated with numerous health outcomes, including bone disease, cancer, autoimmune disease, cardiovascular conditions and more. However, the causal role of vitamin D beyond its importance for bone health remains unclear and is under much debate.
Twin and familial studies from past decades have demonstrated a nontrivial heritability of circulating vitamin D concentrations.
Several large-scale genome-wide association studies (GWAS) have discovered associations of GC, NADSYN1/DHCR7, CYP2R1, CYP24A1, SEC23A, AMDHD1 with serum levels of vitamin D. A recent whole genome sequencing (WGS) study, combined with deep imputation of genome-wide genotyping, has identified a low-frequency synonymous coding variant at CYP2R1. Information on these genetic variants can be used as tools for downstream analysis such as Mendelian randomization. Here, we review the genetic determinants of circulating vitamin D levels by focusing on new findings from GWAS and WGS, as well as results from Mendelian randomization analyses conducted so far for vitamin D with various traits and diseases. The amount of variation in vitamin D explained by genetics is still small, and the putative causal relationship between vitamin D and other diseases remains to be demonstrated.