Neurol Neuroimmunol Neuroinflamm, 7 (2) 2020 Jan 14, DOI: 10.1212/NXI.0000000000000662
Benjamin M Jacobs 1, Alastair J Noyce 1, Gavin Giovannoni 1, Ruth Dobson 2
This appears to examine only those genes which restrict Vitamin Dblood levels
And not those genes which restrict D in the blood getting to the tissues
Example gene: Vitamin D Receptor
Items in both categories Multiple Sclerosis and Vitamin D Receptor are listed here:
- Multiple Sclerosis 2X-3X more likely if poor Vitamin D Receptor – Meta-analysis Feb 2020
- Risk of Multiple Sclerosis varies with the Vitamin D Receptor – meta-analysis Dec 2019
- Multiple Sclerosis and Vitamin D Receptor super enhancers – March 2019
- Vitamin D genes increase MS relapses in children by 2X – May 2019
- Immunological effects of vitamin D and their relations to autoimmunity – March 2019
- Inflammation and immune responses to Vitamin D (perhaps need to measure active vitamin D) – July 2017
- Multiple Sclerosis more likely if poor vitamin D genes - 22nd study – Aug 2017
- Multiple sclerosis (relapsing-remitting) increases activation of Vitamin D Receptor by 6.6 X – March 2017
- Multiple Sclerosis is more likely if poor Vitamin D Receptor (4X Mexico, 3X Iran)– Feb 2017
- Multiple Sclerosis much more likely if poor Vitamin D Receptor – several studies
- Multiple Sclerosis and the Vitamin D Receptor – meta-analysis July 2014
There would have been an even stronger causation factor for Vitamin D if the other genes has also been considered
Vitamin D Receptor activation can be increased by any of: Resveratrol, Omega-3, Magnesium, Zinc, Quercetin, non-daily Vit D, Curcumin, intense exercise, Ginger, Essential oils, etc Note: The founder of VitaminDWiki uses 10 of the 12 known VDR activators
Objective: To update the causal estimates for the effects of adult body mass index (BMI), childhood BMI, and vitamin D status on multiple sclerosis (MS) risk.
Methods: We used 2-sample Mendelian randomization to determine causal estimates. Summary statistics for SNP associations with traits of interest were obtained from the relevant consortia. Primary analyses consisted of random-effects inverse-variance-weighted meta-analysis, followed by secondary sensitivity analyses.
Results: Genetically determined increased childhood BMI (ORMS 1.24, 95% CI 1.05-1.45, p = 0.011) and adult BMI (ORMS 1.14, 95% CI 1.01-1.30, p = 0.042) were associated with increased MS risk. The effect of genetically determined adult BMI on MS risk lessened after exclusion of 16 variants associated with childhood BMI (ORMS 1.11, 95% CI 0.97-1.28, p = 0.121). Correcting for effects of serum vitamin D in a multivariate analysis did not alter the direction or significance of these estimates. Each genetically determined unit increase in the natural-log-transformed vitamin D level was associated with a 43% decrease in the odds of MS (OR 0.57, 95% CI 0.41-0.81, p = 0.001).
Conclusions: We provide novel evidence that BMI before the age of 10 is an independent causal risk factor for MS and strengthen evidence for the causal role of vitamin D in the pathogenesis of MS.