Bonekey Rep. 2014 Mar 5;3:510. doi: 10.1038/bonekey.2014.5. eCollection 2014.
Feldman D1, J Malloy P2.
1 Department of Medicine, Stanford University , Stanford, CA, USA.
2 Department of Pediatrics, Stanford University , Stanford, CA, USA.
Hereditary Vitamin D-resistant rickets is a form which is not treated by Vitamin D
Perhaps Resveratrol, Boron, Zinc, Magnesium etc, which improve the VDR, could be used to treat Hereditary Vitamin D-resistant rickets
Search VitaminDWiki for "RESISTANT RICKETS 195 items as of Dec 2018
Vitamin D Receptor category has the following
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 has a poor VDR (40% of the Obese )
A poor VDR increases the risk of 51 health problems click here for details
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:
|1) Vitamin D supplement|
Sun, Ultraviolet -B
| Vitamin D in the blood |
and thus to the cells
|2) Magnesium||Vitamin D in the blood |
AND to the cells
|3) Omega-3||Vitamin D to the cells|
|4) Resveratrol||Vitamin D to the cells|
|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|
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
Overview of Rickets and vitamin D contains the following summary
Vitamin D deficiency is the cause of most rickets
Rate of rickets is usually < 0.1% of births, unless dark skin or breastfed
Rate of rickets has greatly increased with the drop in vitamin D levels during the past 40 years
400 IU can prevent/treat most rickets (Turkey gave vitamin D to EVERY child)
More than 400 IU may be needed
A low serum level of vitamin D does not indicate rickets
Rate of rickets in some countries varies from 10% to 70% (typically poor health overall)
Rickets was identified 400 years ago and treatments were determined 100 years ago
Rickets is strongly associated with severe breathing problems (weak ribs)
Bowed legs is not the primary indication of rickets (3 other indications of rickets are seen more often)
Heterogeneous loss of function mutations in the vitamin D receptor (VDR) interfere with vitamin D signaling and cause hereditary vitamin D-resistant rickets (HVDRR). HVDRR is characterized by hypocalcemia, secondary hyperparathyroidism and severe early-onset rickets in infancy and is often associated with consanguinity. Affected children may also exhibit alopecia of the scalp and total body. The children usually fail to respond to treatment with calcitriol; in fact, their endogenous levels are often very elevated. Successful treatment requires reversal of hypocalcemia and secondary hyperparathyroidism and is usually accomplished by administration of high doses of calcium given either intravenously or sometimes orally to bypass the intestinal defect in VDR signaling.
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