Neurology. 2016 Dec 13;87(24):2567-2574. Epub 2016 Nov 16.
Mokry LE1, Ross S1, Morris JA1, Manousaki D1, Forgetta V1, Richards JB2.
1From the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
2From the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK. brent.richards at mcgill.ca.
- This study only looked at the genes which affect Vitamin D levels and found a 25% increase
- They failed to look at the 6 additional genes which restrict vitamin D from getting to cells, but which do not restrict vitamin D in the blood
- The study below just looked at the Vitamin D Receptor and found a 300% increase in Alzheimer’s for people with poor VDR, which appears to be a 12 times larger influence
See also VitaminDWiki
Items in BOTH the categories Cognition and Vitamin D Receptor Gene
- Alzheimer’s is associated with all 7 of the genes which restrict vitamin D from getting to tissues – Sept 2018
- Alzheimer’s (1.2X) and Parkenson’s (1.3X) more likely if poor Vitamin D Receptor – meta-analysis March 2019
- Treating herpes reduced incidence of senile dementia by 10 X (HSV1 reduces VDR by 8X) – 2018
- Body may change gene activation if more Vitamin D is needed by tissue (Schiz. in this case) – Oct 2018
- Alzheimer’s associated with Vitamin D and Vitamin D receptor – video and pdf – Aug 2018
- Cerebral small vessel disease 2.5 X more likely if poor Vitamin D Receptor – Sept 2018
- Alzheimer’s Disease is associated with genes which restrict vitamin D – Aug 2015
- Parkinson's and Alzheimer's: associations with vitamin D receptor genes and race – meta-analysis July 2014
- Alzheimer’s patients 3X more likely to have a malfunctioning vitamin D receptor gene – 2012
- Alzheimer’s patients are genetically 70 percent more likely to be vitamin D in-efficient – Feb 2012
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 52 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
To test whether genetically decreased vitamin D levels are associated with Alzheimer disease (AD) using mendelian randomization (MR), a method that minimizes bias due to confounding or reverse causation.
We selected single nucleotide polymorphisms (SNPs) that are strongly associated with 25-hydroxyvitamin D (25OHD) levels (p < 5 × 10-8) from the Study of Underlying Genetic Determinants of Vitamin D and Highly Related Traits (SUNLIGHT) Consortium (N = 33,996) to act as instrumental variables for the MR study. We measured the effect of each of these SNPs on 25OHD levels in the Canadian Multicentre Osteoporosis Study (CaMos; N = 2,347) and obtained the corresponding effect estimates for each SNP on AD risk from the International Genomics of Alzheimer's Project (N = 17,008 AD cases and 37,154 controls). To produce MR estimates, we weighted the effect of each SNP on AD by its effect on 25OHD and meta-analyzed these estimates using a fixed-effects model to provide a summary effect estimate.
The SUNLIGHT Consortium identified 4 SNPs to be genome-wide significant for 25OHD, which described 2.44% of the variance in 25OHD in CaMos. All 4 SNPs map to genes within the vitamin D metabolic pathway. MR analyses demonstrated that a 1-SD decrease in natural log-transformed 25OHD increased AD risk by 25% (odds ratio 1.25, 95% confidence interval 1.03-1.51, p = 0.021). After sensitivity analysis in which we removed SNPs possibly influenced by pleiotropy and population stratification, the results were largely unchanged.
Our results provide evidence supporting 25OHD as a causal risk factor for AD. These findings provide further rationale to understand the effect of vitamin D supplementation on cognition and AD risk in randomized controlled trials.
PMID: 27856775 DOI: 10.1212/WNL.0000000000003430
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