Photochem Photobiol Sci. 2017 Jan 31. doi: 10.1039/c6pp00329j. [Epub ahead of print]
Abstract failed to mention additional restrictions due Vitamin D Receptor, lack of co-factors, etc.
- Vitamin D Cofactors in a nutshell
- Reasons for low response to vitamin D
Such as: low Magnesium, low Boron, smoking, soft drinks, Anemia, darker skin, elderly . . .
Genetics category listing contains the following
410 articles in Vitamin D Receptor 146 articles in Vitamin D Binding Protein = GC 38 articles in CYP27B1
- Calcitriol category listing has
- Topical Vitamin D
- Nanoemulsion Vitamin D may be a substantially better form
- Getting Vitamin D into your body
Vitamin D blood test misses a lot
- Snapshot of the literature by VitaminDWiki 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
- 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
Vitamin D Receptor category has the following
410 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 )
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:
Increasing Increases 1) Vitamin D supplement
Sun, Ultraviolet -B
Vitamin D in the blood
and thus in the cells
2) Magnesium Vitamin 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
Vitamin D Receptor 7) Quercetin (flavonoid) Vitamin D Receptor 8) Zinc is in the VDR Vitamin D Receptor 9) Boron Vitamin D Receptor ?,
10) Essential oils e.g. ginger, curcumin Vitamin D Receptor 11) Progesterone Vitamin D Receptor 12) Infrequent high concentration Vitamin D
Increases the concentration gradient
Vitamin D in the cells 13) Sulfroaphane and perhaps sulfur Vitamin 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
Click on chart for details
- Normal weight Obese (50 ng = 125 nanomole)
Items in both of the categories of Genetics AND Obesity
- High-fat diet reduces CYP2R1 gene needed to make semi-activated vitamin D (mice) – Aug 2021
- Hypothesis: Obesity reduces Vitamin D production by repressing CYP2R1 gene in liver and fat tissue – July 2020
- Increased risk of weight gain when gene restricts Vitamin D getting to tissues (CYP24A1 in this case) – Nov 2019
- Obesity associated with poor Vitamin D genes (VDR in this study) – Jan 2018
- Gut genes related to important disease changed in Obese with 2,000 IU for 12 weeks – May 2019
- Obesity cut semi-activation of Vitamin D in half (mice) – Jan 2019
- Obesity might be related to Vitamin D genes – July 2018
- Vitamin D restricted in getting to cells by genes, obesity, etc – Jan 2017
- Multiple Sclerosis and obesity share some gene problems (as well as low vitamin D) – June 2016
- Vitamin D may block the obesity gene (FTO) – Jan 2014
- Vitamin D roles in obesity: genetics and cell signaling – June 2013
- Obese have 50 percent less of two enzymes in fatty tissue to process vitamin D – May 2013
- No apparent genetic association between vitamin D and obesity – Feb 2013
- Genes indicate that Obesity causes vitamin D deficiency – Feb 2013
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 PDFVitamin D restricted in getting to cells by genes, obesity, etc – Jan 2017
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