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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]

VitaminDWiki

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

Genetics category listing contains the following

331 articles in the Genetics category

see also

Vitamin D blood test misses a lot
in Visio for 2023

  • 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

Vitamin D Receptor category has the following

510 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

See also: 47 studies in the Resveratrol category

It appears that 30% of the population have a poor VDR (40% of the Obese )
Several diseases protect themselves by deactivating the Vitamin D receptor. Example: Breast Cancer
- - - - - - - -
The Vitamin D Receptor is associated with many health problems

Health problems include: Autoimmune (19 studies), Breast Cancer (22 studies), Colon Cancer (13 studies), Cardiovascular (23 studies), Cognition (16 studies), Diabetes (24 studies), Hypertension (9 studies), Infant (21 studies), Lupus (6 studies), Metabolic Syndrome (4 studies), Mortality (4 studies), Multiple Sclerosis (12 studies), Obesity (16 studies), Pregnancy (24 studies), Rheumatoid Arthritis (10 studies), TB (8 studies), VIRUS (36 studies),   Click here for details
Some health problems, such as Breast Cancer, Diabetes, and COVID protect themselves by reducing VDR activation

55 health problems associated with poor VDR


A poor VDR is associated with the risk of 55 health problems  click here for details
The risk of 48 diseases at least double with poor VDR as of Jan 2023  click here for details
Some health problem, such as Breast Cancer reduce the VDR

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


How to increase VDR activation


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 Receptor
13) Sulfroaphane and perhaps sulfurVitamin D Receptor
14)Butyrate especially gutVitamin 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 that 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
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