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Vitamin D restricted in getting to cells by genes, obesity, etc – Jan 2017

Sunlight exposure is just one of the factors which influence vitamin D status.

Photochem Photobiol Sci. 2017 Jan 31. doi: 10.1039/c6pp00329j. [Epub ahead of print]

Vitamin D Life

Abstract failed to mention additional restrictions due Vitamin D Receptor, lack of co-factors, etc.

Genetics category listing contains the following

266 articles in the Genetics category

see also

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

  • Snapshot of the literature by Vitamin D Life as of early 2019
  • 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 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

Vitamin D Receptor category has the following

384 studies in Vitamin D Receptor category

Vitamin D tests cannot detect Vitamin D Receptor (VDR) problems
A poor VDR restricts Vitamin D from getting in the cells
It appears that 30% of the population have a poor VDR (40% of the Obese )

A poor VDR increases the risk of 55 health problems  click here for details
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019

VDR at-home test $29 - results not easily understood in 2016
There are hints that you may have inherited a poor VDR

Compensate for poor VDR by increasing one or more:

IncreasingIncreases
1) Vitamin D supplement
  Sun, Ultraviolet -B
Vitamin D in the blood
and thus in the cells
2) MagnesiumVitamin D in the blood
 AND in the cells
3) Omega-3 Vitamin D in the cells
4) Resveratrol Vitamin D Receptor
5) Intense exercise Vitamin D Receptor
6) Get prescription for VDR activator
   paricalcitol, maxacalcitol?
Vitamin D Receptor
7) Quercetin (flavonoid) Vitamin D Receptor
8) Zinc is in the VDRVitamin D Receptor
9) BoronVitamin D Receptor ?,
etc
10) Essential oils e.g. ginger, curcuminVitamin D Receptor
11) ProgesteroneVitamin D Receptor
12) Infrequent high concentration Vitamin D
Increases the concentration gradient
Vitamin D in the cells
13) Sulfroaphone and perhaps sulfurVitamin D Receptor

Note: If you are not feeling enough benefit from Vitamin D, you might try increasing VDR activation. You might feel the benefit within days of adding one or more of the above

Far healthier and stronger at age 72 due to supplements Includes 6 supplements which help the VDR

Obese need 2.5X more vitamin D

Image

  • Normal weight     Obese     (50 ng = 125 nanomole)

Click here to see the 2014 study

Reductions before Vitamin D gets to the cells

Reductions in Vitamin D is.gd/VitDReductions

Click on chart for details

Items in both of the categories of Genetics AND Obesity


Abboud M1, Rybchyn MS2, Rizk R3, Fraser DR4, Mason RS2.

  • 1Physiology, School of Medical Sciences, Sydney Medical School, Australia. rebecca.mason at sydney.edu.au and Bosch Institute for Medical Research, Australia and College of Sustainability Sciences and Humanities-Zayed University, Abu Dhabi, United Arab Emirates.
  • 2Physiology, School of Medical Sciences, Sydney Medical School, Australia. rebecca.mason at sydney.edu.au and Bosch Institute for Medical Research, Australia.
  • 3Department of Health Services Research, CAPHRI School of Public Health and Primary Care, Maastricht University, Maastricht, 6200 MD Maastricht, The Netherlands.
  • 4Faculty of Veterinary Science, University of Sydney, Sydney, NSW 2006, Australia.

Studies on the determinants of vitamin D status have tended to concentrate on input - exposure to ultraviolet B radiation and the limited sources in food. Yet, vitamin D status, determined by circulating concentrations of 25-hydroxyvitamin D (25(OH)D), can vary quite markedly in groups of people with apparently similar inputs of vitamin D.
There are small effects of polymorphisms in the genes for key proteins involved in vitamin D production and metabolism, including

  • 7-dehydrocholesterol reductase, which converts 7-dehydrocholesterol, the precursor of vitamin D, to cholesterol,
  • CYP2R1, the main 25-hydroxylase of vitamin D,
  • GC, coding for the vitamin D binding protein which transports 25(OH)D and other metabolites in blood and
  • CYP24A1, which 24-hydroxylates both 25(OH)D and the hormone, 1,25-dihydroxyvitamin D.

25(OH)D has a highly variable half-life in blood. There is evidence that the half-life of 25(OH)D is affected by calcium intake and some therapeutic agents.
Fat tissue seems to serve as a sink for the parent vitamin D, which is released mainly when there are reductions in adiposity.

Some evidence is presented to support the proposal that skeletal muscle provides a substantial site of sequestration of 25(OH)D, protecting this metabolite from degradation by the liver, which may help to explain why exercise, not just outdoors, is usually associated with better vitamin D status.

PMID: 28139795 DOI: 10.1039/c6pp00329j
Publisher wants £ 42 for the PDF

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