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Vitamin D Heritability: twin studies – 20 percent to 85 percent, GWAS 5 percent – Oct 2018

The genetics of vitamin D.

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

Genetics category listing contains the following

313 articles in the Genetics category

see also

Vitamin D blood test misses a lot
Blood Test Misses a lot (VDW 3439)

  • 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
    2) Slightly increasing Vitamin D shows 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

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.

Created by admin. Last Modification: Monday October 15, 2018 12:45:16 GMT-0000 by admin. (Version 3)

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